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[PMID]:28009705
[Au] Autor:Stevenson ER; Johns EM; Marques FZ; Jackson KL; Davern PJ; Evans RG; Head GA
[Ad] Endereço:aNeuropharmacology Laboratory, Baker IDI Heart and Diabetes Research Institute, Melbourne bDepartment of Pharmacology cDepartment of Cardiovascular Disease Program, Biosciences Discovery Institute and Department of Physiology, Monash University, Clayton, Victoria, Australia.
[Ti] Título:Positive allosteric modulation of GABAA receptors attenuates high blood pressure in Schlager hypertensive mice.
[So] Source:J Hypertens;35(3):546-557, 2017 Mar.
[Is] ISSN:1473-5598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Blood pressure high Schlager (BPH/2J) mice have neurogenic hypertension associated with differences in hypothalamic GABAA receptors compared with their normotensive counterparts (BPN/3J). Allopregnanolone is an endogenous neurosteroid reduced in chronic stress, and when administered, decreases anxiety by positive allosteric modulation of GABAA receptors. METHODS: To determine if allopregnanolone could be a viable therapeutic for neurogenic hypertension, male BPH/2J (n = 6-7) and BPN/3J (n = 8-9) mice were equipped with radiotelemetry probes to compare cardiovascular variables before and after implantation of subcutaneous minipumps delivering allopregnanolone (5 mg/kg per day), or its vehicle, for a period of 2 weeks. In addition to baseline recordings, the response to stress and ganglionic blockade with pentolinium was recorded, before and 7-14 days after minipump implantation. Following treatment, brains were processed for c-Fos immunohistochemistry and quantitative real-time polymerase chain reaction. RESULTS: Administration of allopregnanolone selectively reduced mean arterial pressure (-8.0 ±â€Š2.7 mmHg; P = 0.02) and the depressor response to pentolinium (-15.3 ±â€Š3.2 mmHg; P = 0.001) in BPH/2J mice, with minimal effects observed in BPN/3J mice. Following allopregnanolone treatment, the diminished expression of GABAA δ, α4 and ß2 subunits in the hypothalamus (-1.6 to 4.8-fold; Pstrain < 0.05) was abolished. Furthermore, in BPH/2J mice, allopregnanolone treatment reduced the pressor response to dirty cage switch stress (-26.7 ±â€Š4.5%; P < 0.001) and abolished the elevated c-Fos expression in pre-sympathetic nuclei. CONCLUSION: The selective antihypertensive and stress inhibitory effects of allopregnanolone in BPH/2J mice suggest that allosteric modulation of GABAA receptors, in amygdalo-hypothalamic pathways, may contribute to the development of hypertension in this model and may offer a potential new therapeutic avenue.
[Mh] Termos MeSH primário: Pressão Sanguínea/efeitos dos fármacos
Hipotálamo/metabolismo
Pregnanolona/uso terapêutico
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores de GABA-A/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Expressão Gênica
Hipertensão/tratamento farmacológico
Hipertensão/fisiopatologia
Masculino
Camundongos
Tartarato de Pentolínio/farmacologia
Proteínas Proto-Oncogênicas c-fos/genética
Reação em Cadeia da Polimerase em Tempo Real
Estresse Fisiológico
Sistema Nervoso Simpático/efeitos dos fármacos
Sistema Nervoso Simpático/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, GABA-A); 953357GACY (Pentolinium Tartrate); BXO86P3XXW (Pregnanolone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.1097/HJH.0000000000001210


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[PMID]:27672029
[Au] Autor:Mäki-Petäjä KM; Barrett SM; Evans SV; Cheriyan J; McEniery CM; Wilkinson IB
[Ad] Endereço:From the Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, United Kingdom. km391@medschl.cam.ac.uk.
[Ti] Título:The Role of the Autonomic Nervous System in the Regulation of Aortic Stiffness.
[So] Source:Hypertension;68(5):1290-1297, 2016 Nov.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The autonomic nervous system is important in regulating blood pressure, but whether it regulates aortic stiffness is more contentious. We conducted 3 studies in young, healthy individuals to address this important question. Study 1 was a cross-sectional study of 347 subjects with detailed measurements of hemodynamics and heart rate variability. In study 2, 9 subjects were given a bolus of intravenous nicotinic ganglion blocker, pentolinium, or saline in a random order and hemodynamics and heart rate variability were assessed before and after. In study 3, changes in hemodynamics and heart rate variability were assessed during stimulation of the sympathetic nervous system with the use of isometric handgrip exercise in 12 subjects. Study 1: aortic pulse wave velocity (P=0.003) was lowest in the subjects with the highest parasympathetic activity, but after adjusting for mean arterial pressure, the effect was abolished (P=0.3). Study 2: after pentolinium, sympathetic and parasympathetic activity fell (P=0.001 for both), mean arterial pressure, and heart rate increased (P=0.004 and P=0.04, respectively), but there was no change in pulse wave velocity in comparison to placebo (P=0.1). Study 3: during handgrip exercise, sympathetic activity (P=0.003), mean arterial pressure (P<0.0001), and aortic pulse wave velocity increased (P=0.013). However, pulse wave velocity adjusted for mean arterial pressure did not change (P=0.1). The main finding of these studies is that in young healthy subjects, the autonomic nervous system does not have a pressure-independent role in the regulation of aortic stiffness. However, these findings may not apply to patients with increased sympathetic tone or hypertension.
[Mh] Termos MeSH primário: Pressão Arterial/fisiologia
Sistema Nervoso Autônomo/fisiopatologia
Frequência Cardíaca/fisiologia
Hemodinâmica/fisiologia
Hipertensão/fisiopatologia
Rigidez Vascular/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Estudos Cross-Over
Estudos Transversais
Método Duplo-Cego
Feminino
Força da Mão/fisiologia
Voluntários Saudáveis
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
Masculino
Tartarato de Pentolínio/administração & dosagem
Prognóstico
Análise de Onda de Pulso
Papel (Figurativo)
Rigidez Vascular/fisiologia
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
953357GACY (Pentolinium Tartrate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160928
[St] Status:MEDLINE


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[PMID]:26186712
[Au] Autor:Rajapakse NW; Karim F; Evans RG; Kaye DM; Head GA
[Ad] Endereço:Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Department of Physiology, Monash University, Melbourne, Australia.
[Ti] Título:Augmented Endothelial-Specific L-Arginine Transport Blunts the Contribution of the Sympathetic Nervous System to Obesity Induced Hypertension in Mice.
[So] Source:PLoS One;10(7):e0131424, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Augmenting endothelial specific transport of the nitric oxide precursor L-arginine via cationic amino acid transporter-1 (CAT1) can prevent obesity related hypertension. We tested the hypotheses that CAT1 overexpression prevents obesity-induced hypertension by buffering the influence of the sympathetic nervous system (SNS) on the maintenance of arterial pressure and by buffering pressor responses to stress. Wild type (WT; n=13) and CAT1 overexpressing mice (CAT+; n=13) were fed a normal or a high fat diet for 20 weeks. Mice fed a high fat diet were returned to the control diet before experiments commenced. Baseline mean arterial pressure (MAP) and effects of restraint-, shaker- and almond feeding-stress and ganglionic blockade (pentolinium; 5 mg/kg; i.p.) on MAP were determined in conscious mice. Fat feeding increased body weight to a similar extent in WT and CAT+ but MAP was greater only in WT compared to appropriate controls (by 29%). The depressor response to pentolinium was 65% greater in obese WT than lean WT (P < 0.001), but was similar in obese and lean CAT+ (P = 0.65). In lean WT and CAT+, pressor responses to shaker and feeding stress, but not restraint stress, were less in the latter genotype compared to the former (P ≤ 0.001). Pressor responses to shaker and feeding stress were less in obese WT than lean WT (P ≤ 0.001), but similar in obese and lean CAT+. The increase in MAP in response to restraint stress was less in obese WT (22 ± 2%), but greater in obese CAT+ (37 ± 2%), when compared to respective lean WT (31 ± 3%) and lean CAT+ controls (27 ± 2%; P ≤ 0.02). We conclude that CAT1 overexpression prevents obesity-induced hypertension by reducing the influence of the SNS on the maintenance of arterial pressure but not by buffering pressor responses to stress.
[Mh] Termos MeSH primário: Transportador 1 de Aminoácidos Catiônicos/genética
Gorduras na Dieta/administração & dosagem
Hipertensão/metabolismo
Obesidade/metabolismo
Estresse Psicológico/metabolismo
Sistema Nervoso Simpático/metabolismo
[Mh] Termos MeSH secundário: Animais
Pressão Arterial/efeitos dos fármacos
Transportador 1 de Aminoácidos Catiônicos/metabolismo
Dieta Hiperlipídica
Endotélio Vascular/efeitos dos fármacos
Bloqueadores Ganglionares/farmacologia
Expressão Gênica
Hipertensão/etiologia
Hipertensão/genética
Hipertensão/fisiopatologia
Imobilização
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Obesidade/etiologia
Obesidade/genética
Obesidade/fisiopatologia
Tartarato de Pentolínio/farmacologia
Prunus dulcis/química
Estresse Psicológico/genética
Estresse Psicológico/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
Sistema Nervoso Simpático/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cationic Amino Acid Transporter 1); 0 (Dietary Fats); 0 (Ganglionic Blockers); 0 (Slc7a1 protein, mouse); 953357GACY (Pentolinium Tartrate)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150729
[Lr] Data última revisão:
150729
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150718
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0131424


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[PMID]:25255392
[Au] Autor:Vanecková I; Dobesová Z; Kunes J; Vernerová Z; Zicha J
[Ad] Endereço:aInstitute of Physiology, Academy of Sciences of the Czech Republic bDepartment of Pathology, 3rd Faculty of Medicine, Charles University, Prague, Czech Republic.
[Ti] Título:Endothelin A receptor blocker atrasentan lowers blood pressure by the reduction of nifedipine-sensitive calcium influx in Ren-2 transgenic rats fed a high-salt diet.
[So] Source:J Hypertens;33(1):161-9, 2015 Jan.
[Is] ISSN:1473-5598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Our previous experiments demonstrated that selective endothelin A (ETA) receptor blockade had antihypertensive effects in Ren-2 transgenic rats (TGRs), but the mechanisms responsible for this change of blood pressure (BP) have not been explored yet. METHOD: Four-week-old male heterozygous TGRs and their normotensive controls--Hannover Sprague-Dawley (HanSD) rats--were fed high-salt diet (2% NaCl) and were treated with selective ETA receptor blocker atrasentan (5 mg/kg per day) for 8 weeks. At the end of the study, the contribution of principle vasoactive systems was evaluated by the sequential blockade of the renin-angiotensin system (captopril), sympathetic nervous system (pentolinium) and nitric oxide synthase [N-nitro-L-arginine methyl ester (L-NAME)]. The role of calcium influx through L-type voltage-dependent calcium channels in BP maintenance was evaluated using nifedipine. In a separate group of animals, the efficiency of distinct vasodilator systems--prostanoids (blocked by nonselective cyclooxygenase inhibitor indomethacin) and Ca-activated K channels (inhibited by tetraethylammonium)--was also analyzed. RESULTS: Atrasentan attenuated the development of hypertension in heterozygous TGRs, but had no effects in Hannover Sprague-Dawley rats. Moreover, atrasentan moderately attenuated renin-angiotensin system-dependent vasoconstriction, whereas it had no effect on sympathetic vasoconstriction. The nifedipine-sensitive BP component was markedly decreased by atrasentan treatment. In contrast, vasodilatation mediated by nitric oxide, endogenous prostanoids or Ca-activated K channels was reduced in atrasentan-treated TGRs, indicating the absence of compensatory augmentation of endothelin B receptor-mediated vasodilation in these animals. CONCLUSION: BP-lowering effect of chronic atrasentan treatment in TGRs was mainly caused by reduced Ca influx through L-type voltage-dependent calcium channels due to missing ETA receptor-dependent vasoconstriction and attenuated angiotensin II-dependent vasoconstriction.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Antagonistas do Receptor de Endotelina A/química
Hipertensão/fisiopatologia
Nifedipino/química
Pirrolidinas/uso terapêutico
[Mh] Termos MeSH secundário: Ração Animal
Animais
Anti-Hipertensivos/química
Pressão Sanguínea/fisiologia
Cálcio/química
Canais de Cálcio Tipo L/metabolismo
Captopril/química
Masculino
NG-Nitroarginina Metil Éster/química
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase/metabolismo
Tartarato de Pentolínio/química
Ratos
Ratos Sprague-Dawley
Ratos Transgênicos
Renina/genética
Sistema Renina-Angiotensina/efeitos dos fármacos
Cloreto de Sódio na Dieta/farmacologia
Sistema Nervoso Simpático/fisiopatologia
Vasoconstrição/efeitos dos fármacos
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Calcium Channels, L-Type); 0 (Endothelin A Receptor Antagonists); 0 (Pyrrolidines); 0 (Ren2 protein, rat); 0 (Sodium Chloride, Dietary); 31C4KY9ESH (Nitric Oxide); 953357GACY (Pentolinium Tartrate); 9G64RSX1XD (Captopril); EC 1.14.13.39 (Nitric Oxide Synthase); EC 3.4.23.15 (Renin); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); V55S2QJN2X (NG-Nitroarginine Methyl Ester); V6D7VK2215 (atrasentan)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:141204
[Lr] Data última revisão:
141204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140926
[St] Status:MEDLINE
[do] DOI:10.1097/HJH.0000000000000357


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[PMID]:24446057
[Au] Autor:Jackson KL; Palma-Rigo K; Nguyen-Huu TP; Davern PJ; Head GA
[Ad] Endereço:Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Research Institute, 75 Commercial Rd, Melbourne, Vic, 3004, Australia. geoff.head@baker.edu.au.
[Ti] Título:Major contribution of the medial amygdala to hypertension in BPH/2J genetically hypertensive mice.
[So] Source:Hypertension;63(4):811-8, 2014 Apr.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BPH/2J mice are recognized as a neurogenic model of hypertension primarily based on overactivity of the sympathetic nervous system and greater neuronal activity in key autonomic cardiovascular regulatory brain regions. The medial amygdala (MeAm) is a forebrain region that integrates the autonomic response to stress and is the only region found to have greater Fos during the night and daytime in BPH/2J compared with BPN/3J mice. To determine the contribution of the MeAm to hypertension, the effect of neuronal ablation on blood pressure (BP) was assessed in BPH/2J (n=7) and normotensive BPN/3J mice (n=7). Mice were preimplanted with radiotelemetry devices to measure 24-hour BP and cardiovascular responses to stress, before and 1 to 3 weeks after bilateral lesions of the MeAm. Baseline BP was 121±4 mm Hg in BPH/2J and 101±2 mm Hg in BPN/3J mice (Pstrain<0.001). MeAm lesions reduced BP by 11±2 mm Hg in BPH/2J mice (Plesion<0.001) but had no effect in BPN/3J mice. The hypotensive effect of lesions in BPH/2J mice was similar during both day and night, suggesting that the MeAm has tonic effects on BP, but the pressor response to stress was maintained in both strains. Midfrequency BP power was attenuated in both strains (Plesion<0.05) and the depressor responses to pentolinium after enalaprilat pretreatment was attenuated after lesions in BPH/2J mice (Plesion<0.001; n=3). These findings indicate that the MeAm provides a tonic contribution to hypertension in BPH/2J mice, which is independent of its role in stress reactivity or circadian BP influences.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/fisiologia
Modelos Animais de Doenças
Hipertensão/genética
Hipertensão/fisiopatologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/efeitos dos fármacos
Animais
Pressão Sanguínea/fisiologia
Ritmo Circadiano/fisiologia
Enalaprilate/farmacologia
Masculino
Camundongos
Camundongos Mutantes
Tartarato de Pentolínio/farmacologia
Sistema Nervoso Simpático/efeitos dos fármacos
Sistema Nervoso Simpático/fisiologia
Telemetria
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
953357GACY (Pentolinium Tartrate); GV0O7ES0R3 (Enalaprilat)
[Em] Mês de entrada:1406
[Cu] Atualização por classe:160726
[Lr] Data última revisão:
160726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140122
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.113.02020


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[PMID]:24270178
[Au] Autor:Davern PJ; Chowdhury S; Jackson KL; Nguyen-Huu TP; Head GA
[Ad] Endereço:aNeuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne bDepartment of Pharmacology, Monash University, Clayton, Victoria, Australia.
[Ti] Título:GABAA receptor dysfunction contributes to high blood pressure and exaggerated response to stress in Schlager genetically hypertensive mice.
[So] Source:J Hypertens;32(2):352-62, 2014 Feb.
[Is] ISSN:1473-5598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Schlager BPH/2J hypertensive mice have high blood pressure (BP) likely due to overactivity of the sympathetic nervous system regulated by neurons in amygdala-hypothalamic pathways. These areas are normally under tonic inhibition by GABA containing neurons that may be deficient in Schlager hypertensive mice as suggested by microarray analysis. In the present study, cardiovascular effects of chronic activation of GABAA receptors were examined in BPH/2J mice. METHODS: Male normotensive BPN/3J and hypertensive BPH/2J mice were administered diazepam in drinking water for 7 days. BP, heart rate and locomotor activity were recorded by telemetry. RESULTS: Diazepam (2.5 mg/kg) reduced BP of BPN/3J mice during the night-time by -7.1 ± 2.0 mmHg (P = 0.001) but had no effect in BPH/2J mice (+2 ± 2 mmHg) and no effect on heart rate or locomotor activity in either strain. Diazepam reduced the responses to restraint stress in BPN/3J mice by 20% (P = 0.01) and there was no association between Fos-immunoreactive neurons and neurons expressing GABAA receptors or neuropeptide Y in the medial amygdala and paraventricular nucleus of the hypothalamus. By contrast diazepam had no effect on the pressor response to stress in BPH/2J mice and ~50% of stress-activated neurons in these regions also expressed GABAA receptors and ~45% were neuropeptide Y-containing. CONCLUSION: These findings show that BPH/2J mice are resistant to the effects of diazepam and suggest that GABAA receptor dysfunction in BPH/2J mice may be contributing to the neurogenic hypertension by not suppressing arousal-induced sympathetic activation within amygdala and hypothalamic nuclei.
[Mh] Termos MeSH primário: Hipertensão/etiologia
Receptores de GABA-A/fisiologia
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/metabolismo
Animais
Barorreflexo/efeitos dos fármacos
Barorreflexo/fisiologia
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/genética
Pressão Sanguínea/fisiologia
Diazepam/administração & dosagem
Moduladores GABAérgicos/administração & dosagem
Bloqueadores Ganglionares/farmacologia
Hipertensão/genética
Hipertensão/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos
Neuropeptídeo Y/metabolismo
Núcleo Hipotalâmico Paraventricular/metabolismo
Tartarato de Pentolínio/farmacologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
Restrição Física
Estresse Fisiológico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (GABA Modulators); 0 (Ganglionic Blockers); 0 (Neuropeptide Y); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, GABA-A); 953357GACY (Pentolinium Tartrate); Q3JTX2Q7TU (Diazepam)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:140116
[Lr] Data última revisão:
140116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131126
[St] Status:MEDLINE
[do] DOI:10.1097/HJH.0000000000000015


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[PMID]:23897069
[Au] Autor:Jackson KL; Marques FZ; Watson AM; Palma-Rigo K; Nguyen-Huu TP; Morris BJ; Charchar FJ; Davern PJ; Head GA
[Ad] Endereço:Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Research Institute, P.O. Box 6492, St Kilda Rd Central, Melbourne, Victoria 8008, Australia. geoff.head@baker.edu.au.
[Ti] Título:A novel interaction between sympathetic overactivity and aberrant regulation of renin by miR-181a in BPH/2J genetically hypertensive mice.
[So] Source:Hypertension;62(4):775-81, 2013 Oct.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genetically hypertensive mice (BPH/2J) are hypertensive because of an exaggerated contribution of the sympathetic nervous system to blood pressure. We hypothesize that an additional contribution to elevated blood pressure is via sympathetically mediated activation of the intrarenal renin-angiotensin system. Our aim was to determine the contribution of the renin-angiotensin system and sympathetic nervous system to hypertension in BPH/2J mice. BPH/2J and normotensive BPN/3J mice were preimplanted with radiotelemetry devices to measure blood pressure. Depressor responses to ganglion blocker pentolinium (5 mg/kg i.p.) in mice pretreated with the angiotensin-converting enzyme inhibitor enalaprilat (1.5 mg/kg i.p.) revealed a 2-fold greater sympathetic contribution to blood pressure in BPH/2J mice during the active and inactive period. However, the depressor response to enalaprilat was 4-fold greater in BPH/2J compared with BPN/3J mice, but only during the active period (P=0.01). This was associated with 1.6-fold higher renal renin messenger RNA (mRNA; P=0.02) and 0.8-fold lower abundance of micro-RNA-181a (P=0.03), identified previously as regulating human renin mRNA. Renin mRNA levels correlated positively with depressor responses to pentolinium (r=0.99; P=0.001), and BPH/2J mice had greater renal sympathetic innervation density as identified by tyrosine hydroxylase staining of cortical tubules. Although there is a major sympathetic contribution to hypertension in BPH/2J mice, the renin-angiotensin system also contributes, doing so to a greater extent during the active period and less during the inactive period. This is the opposite of the normal renin-angiotensin system circadian pattern. We suggest that renal hyperinnervation and enhanced sympathetically induced renin synthesis mediated by lower micro-RNA-181a contributes to hypertension in BPH/2J mice.
[Mh] Termos MeSH primário: Hipertensão/genética
MicroRNAs/genética
Sistema Renina-Angiotensina/fisiologia
Renina/sangue
Sistema Nervoso Simpático/fisiopatologia
[Mh] Termos MeSH secundário: Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Enalaprilate/farmacologia
Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/fisiologia
Hipertensão/sangue
Hipertensão/fisiopatologia
Camundongos
Atividade Motora/efeitos dos fármacos
Atividade Motora/fisiologia
Antagonistas Nicotínicos/farmacologia
Tartarato de Pentolínio/farmacologia
Sistema Renina-Angiotensina/efeitos dos fármacos
Sistema Nervoso Simpático/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (MicroRNAs); 0 (Nicotinic Antagonists); 0 (mirn181 microRNA, mouse); 953357GACY (Pentolinium Tartrate); EC 3.4.23.15 (Renin); GV0O7ES0R3 (Enalaprilat)
[Em] Mês de entrada:1312
[Cu] Atualização por classe:160726
[Lr] Data última revisão:
160726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130731
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.113.01701


  8 / 371 MEDLINE  
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[PMID]:23887975
[Au] Autor:Abegaz B; Davern PJ; Jackson KL; Nguyen-Huu TP; Bassi JK; Connelly A; Choong YT; Allen AM; Head GA
[Ad] Endereço:Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Research Institute, Melbourne, Victoria 8008, Australia.
[Ti] Título:Cardiovascular role of angiotensin type1A receptors in the nucleus of the solitary tract of mice.
[So] Source:Cardiovasc Res;100(2):181-91, 2013 Nov 01.
[Is] ISSN:1755-3245
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: The nucleus of the solitary tract (NTS) is important for cardiovascular regulation and contains angiotensin type 1A (AT1A) receptors. To assess its function, we examined the effect of expressing in AT1A receptors in the NTS of mice lacking these receptors. METHODS AND RESULTS: Bilateral microinjections of lentivirus expressing AT1A receptors (AT1Av mice, n = 6) or green fluorescent protein (GFPv, n = 8, control) under the control of the PRSx8 promotor were made into the NTS of AT1A receptors null mice (AT1A(-/-)). Telemetry devices recorded blood pressure (BP), heart rate (HR), and locomotor activity. Expression of AT1A receptors in the NTS increased BP by 11.2 ± 4 mmHg (P < 0.05) at 2 and 3 weeks, whereas GFPv mice remained at pre-injection BP. Ganglion blockade reduced BP to similar levels pre- and post-transfection in GFPv and AT1Av mice. Greater pressor responses to cage-switch stress were observed following AT1A receptors expression (+18 ± 2 mmHg pre- to +24 ± 2 mmHg post-virus, P < 0.05) with similar stress-induced pressor responses pre- and post-virus in GFPv mice. Pressor responses to restraint stress pre- and post-virus were similar in AT1Av but were 20% less post-GFPv (P < 0.001). The lack of attenuation in BP to restraint was associated with four-fold greater Fos-expression in AT1A receptors mice. AT1A receptors expression in the NTS did not alter baroreflex gain differently between groups. CONCLUSION: The results suggest that transfection of AT1A receptors on neurons in the NTS elevates BP independent of the SNS and pressor responses to aversive stimuli are associated with greater Fos-expression in forebrain regions. This study suggests a novel mechanism by which the NTS may modulate MAP in the long-term via AT1A receptors.
[Mh] Termos MeSH primário: Pressão Arterial/fisiologia
Frequência Cardíaca/fisiologia
Receptor Tipo 1 de Angiotensina/fisiologia
Núcleo Solitário/fisiologia
[Mh] Termos MeSH secundário: Animais
Autorradiografia
Barorreflexo
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Atividade Motora
Tartarato de Pentolínio/farmacologia
Proteínas Proto-Oncogênicas c-fos/análise
Estresse Psicológico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-fos); 0 (Receptor, Angiotensin, Type 1); 953357GACY (Pentolinium Tartrate)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:131017
[Lr] Data última revisão:
131017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130727
[St] Status:MEDLINE
[do] DOI:10.1093/cvr/cvt183


  9 / 371 MEDLINE  
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[PMID]:22425821
[Au] Autor:Chan YL; Orie NN; Dyson A; Taylor V; Stidwill RP; Clapp LH; Singer M
[Ad] Endereço:Bloomsbury Institute of Intensive Care Medicine, Centre for Clinical Pharmacology and Therapeutics, Division of Medicine, University College London, UK.
[Ti] Título:Inhibition of vascular adenosine triphosphate-sensitive potassium channels by sympathetic tone during sepsis.
[So] Source:Crit Care Med;40(4):1261-8, 2012 Apr.
[Is] ISSN:1530-0293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Excessive opening of the adenosine triphosphate-sensitive potassium channel in vascular smooth muscle is implicated in the vasodilation and vascular hyporeactivity underlying septic shock. Therapeutic channel inhibition using sulfonylurea agents has proved disappointing, although agents acting on its pore appear more promising. We thus investigated the hemodynamic effects of adenosine triphosphate-sensitive potassium channel pore inhibition in awake, fluid-resuscitated septic rats, and the extent to which these responses are modulated by the high sympathetic tone present in sepsis. Temporal changes in ex-vivo channel activity and subunit gene expression were also investigated. DESIGN: In vivo and ex vivo animal study. SETTING: University research laboratory. SUBJECTS: Male adult Wistar rats. INTERVENTIONS AND MEASUREMENTS: Fecal peritonitis was induced in conscious, fluid-resuscitated rats. Pressor responses to norepinephrine and PNU-37883A (a vascular adenosine triphosphate-sensitive potassium channel inhibitor acting on the Kir6.1 pore-forming subunit) were measured at 6 or 24 hrs, in the absence or presence of the autonomic ganglion blocker, pentolinium. The aorta and mesenteric artery were examined ex vivo for rubidium efflux as a marker of adenosine triphosphate-sensitive potassium channel activity, and for adenosine triphosphate-sensitive potassium channel subunit gene expression using quantitative reverse transcription-polymerase chain reaction. MAIN RESULTS: A total of 120 rats (50 sham-operated controls, 70 septic) were included. Septic rats became hypotensive after 12 hrs, with a 24-hr mortality of 51.7% (0% in controls). At 6 hrs, there was an attenuated pressor response to norepinephrine (p < .01) despite blood pressure being elevated (p < .01). PNU-37883A had no pressor effect, except in the presence of pentolinium (p < .01). Kir6.1 subunit mRNA increased significantly in the mesenteric artery while rubidium efflux was increased in both the aorta and mesenteric artery at 24 hrs. CONCLUSIONS: Despite evidence of increased adenosine triphosphate-sensitive potassium channel activity in sepsis, it appears to be inhibited in vivo by high sympathetic tone. This may explain, at least in part, the reduced efficacy of adenosine triphosphate-sensitive potassium channel blockers in human septic shock.
[Mh] Termos MeSH primário: Vasos Sanguíneos/fisiopatologia
Sepse/fisiopatologia
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adamantano/análogos & derivados
Adamantano/farmacologia
Animais
Aorta/efeitos dos fármacos
Aorta/fisiopatologia
Vasos Sanguíneos/efeitos dos fármacos
Vasos Sanguíneos/metabolismo
Bloqueadores Ganglionares/farmacologia
Expressão Gênica/efeitos dos fármacos
Expressão Gênica/fisiologia
Masculino
Artérias Mesentéricas/efeitos dos fármacos
Artérias Mesentéricas/fisiopatologia
Morfolinas/farmacologia
Norepinefrina/farmacologia
Tartarato de Pentolínio/farmacologia
Ratos
Ratos Wistar
Sepse/metabolismo
ATPase Trocadora de Sódio-Potássio/metabolismo
ATPase Trocadora de Sódio-Potássio/fisiologia
Vasodilatação/efeitos dos fármacos
Vasodilatação/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ganglionic Blockers); 0 (Morpholines); 57568-80-6 (U 37883A); 953357GACY (Pentolinium Tartrate); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); PJY633525U (Adamantane); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1205
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:120320
[St] Status:MEDLINE
[do] DOI:10.1097/CCM.0b013e31823da98d


  10 / 371 MEDLINE  
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[PMID]:21535246
[Au] Autor:Fortaleza EA; Scopinho AA; Corrêa FM
[Ad] Endereço:Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Bandeirantes Avenue 3900, Ribeirão Preto, SP 14049-900, Brazil.
[Ti] Título:Cardiovascular responses to microinjection of noradrenaline into the medial amygdaloid nucleus of conscious rats result from α2-receptor activation and vasopressin release.
[So] Source:Eur J Neurosci;33(9):1677-84, 2011 May.
[Is] ISSN:1460-9568
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:The medial amygdaloid nucleus (MeA) is involved in the modulation of physiological and behavioral processes, as well as regulation of the autonomic nervous system. Moreover, MeA electrical stimulation evokes cardiovascular responses. Thus, as noradrenergic receptors are present in this structure, the present study tested the effects of local noradrenaline (NA) microinjection into the MeA on cardiovascular responses in conscious rats. Moreover, we describe the types of adrenoceptor involved and the peripheral mechanisms involved in the cardiovascular responses. Increasing doses of NA (3, 9, 27 or 45 nmol/100 nL) microinjected into the MeA of conscious rats caused dose-related pressor and bradycardic responses. The NA cardiovascular effects were abolished by local pretreatment of the MeA with 10 nmol/100 nL of the specific α2-receptor antagonist RX821002, but were not affected by local pretreatment with 10 nmol/100 nL of the specific α1-receptor antagonist WB4101. The magnitude of pressor response evoked by NA microinjected into the MeA was potentiated by intravenous pretreatment with the ganglion blocker pentolinium (5 mg/kg), and blocked by intravenous pretreatment with the selective V1-vasopressin antagonist dTyr(CH2)5 (Me)AVP (50 µg/kg). In conclusion, our results show that microinjection of NA into the MeA of conscious rats activates local α2-adrenoceptors, evoking pressor and bradycardic responses, which are mediated by vasopressin release.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/efeitos dos fármacos
Tonsila do Cerebelo/metabolismo
Norepinefrina/farmacologia
Receptores Adrenérgicos alfa 2/metabolismo
Vasopressinas/metabolismo
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos alfa/farmacologia
Tonsila do Cerebelo/anatomia & histologia
Animais
Dioxanos/farmacologia
Masculino
Microinjeções
Antagonistas Nicotínicos/farmacologia
Tartarato de Pentolínio/farmacologia
Ratos
Ratos Wistar
Vasoconstritores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic alpha-Antagonists); 0 (Dioxanes); 0 (Nicotinic Antagonists); 0 (Receptors, Adrenergic, alpha-2); 0 (Vasoconstrictor Agents); 11000-17-2 (Vasopressins); 953357GACY (Pentolinium Tartrate); E9H51OIT2B ((2-(2',6'-dimethoxy)phenoxyethylamino)methylbenzo-1,4-dioxane); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1109
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110504
[St] Status:MEDLINE
[do] DOI:10.1111/j.1460-9568.2011.07655.x



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