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[PMID]:29216197
[Au] Autor:Yeh CC; Fan Y; Xu Y; Yang YL; Simpson PC; Mann MJ
[Ad] Endereço:Cardiothoracic Translational Research Laboratory, University of California San Francisco, San Francisco, California, United States of America.
[Ti] Título:Shift toward greater pathologic post-myocardial infarction remodeling with loss of the adaptive hypertrophic signaling of alpha1 adrenergic receptors in mice.
[So] Source:PLoS One;12(12):e0188471, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: We have hypothesized that post-infarction cardiac remodeling can be influenced by shifts in the balance between intracellular mediators of "pathologic" and "physiologic" hypertrophy. Although alpha1 adrenergic receptors (alpha1-ARs) mediate pro-adaptive hypertrophy during pressure overload, little is known about their role or downstream mediators after myocardial infarction. METHODS: We performed loss-of-function experiments via coronary ligation in alpha1A-AR knockout (AKO) mice. Post-myocardial infarction (MI) remodeling was evaluated via echocardiography, quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis of cardiac fetal gene expression, histologic analysis of myocyte size, post-MI fibrosis and apoptosis, and Western blot analysis of apoptotic regulators. RESULTS: Alpha1A-AR knockout paradoxically increased post-MI hypertrophy compared to wild type controls (WT), but also increased ventricular dilatation, fibrosis, apoptosis, and 4-week post-MI mortality (64% in AKO vs. 25% in WT, P = 0.02), suggesting a shift toward greater pathologic hypertrophy in the absence of pro-adaptive alpha1A effects. alpha1A-AR knockout increased phospho-p38 levels in the pre-MI myocardium compared to WT (0.55 ± 0.16 vs. 0.03 ± 0.01, P<0.05) but decreased phospho-ERK1/2 post-MI (0.49 ± 0.35 arbitrary units vs. 1.55 ± 0.43 in WT, P<0.05). Furthermore, expression of pro-apoptotic factor Bax was increased (1.19 ± 0.15 vs. 0.78 ± 0.08, P<0.05) and expression of anti-apoptotic factors Bcl2 was decreased (0.26 ± 0.01 vs. 0.55 ± 0.06, P<0.01) compared to WT. CONCLUSIONS: Alpha1A-AR provides an important counterbalance to pathologic pathways during post-MI remodeling that may be mediated through ERK1/2 signaling; these observations provide support for further development of an alpha1A-AR/ERK-based molecular intervention for this chronic, often fatal disease.
[Mh] Termos MeSH primário: Sistema de Sinalização das MAP Quinases
Infarto do Miocárdio/patologia
Receptores Adrenérgicos alfa 1/fisiologia
Remodelação Ventricular
[Mh] Termos MeSH secundário: Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Captopril/farmacologia
Masculino
Camundongos
Camundongos Knockout
Receptores Adrenérgicos alfa 1/genética
Receptores Adrenérgicos alfa 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Receptors, Adrenergic, alpha-1); 9G64RSX1XD (Captopril)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188471


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[PMID]:28827087
[Au] Autor:Smeda JS; Daneshtalab N
[Ad] Endereço:Division of BioMedical Sciences, Memorial University of Newfoundland, St. John's, Newfoundland, Canada. Electronic address: jsmeda@mun.ca.
[Ti] Título:Cerebrovascular recovery after stroke with individual and combined losartan and captopril treatment of SHRsp.
[So] Source:Vascul Pharmacol;96-98:40-52, 2017 Sep.
[Is] ISSN:1879-3649
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We assessed whether the superior restoration of cerebrovascular function after hemorrhagic stroke by losartan versus captopril treatment was due to better BP, uremia, uricaemia, or aldosterone control in Kyoto Wistar stroke-prone-hypertensive rats and evaluated whether elevated angiotensin II (A2) levels enhanced the effectiveness of losartan treatment. Constriction was studied in the middle cerebral arteries (MCAs) using a pressure myograph. Post-stroke survival increased from 21 to 310 and 189days respectively with losartan and captopril treatment. Neither treatment reduced BP, both reversed uremia and hyperaldosteronism equally after 7days. Plasma uric acid remained low. At stroke, MCA constriction to pressure (PDC), protein kinase C (PKC) activation, depolarization, and sarcoplasmic Ca were attenuated. Endothelial-dependent-vasodilation by bradykinin and endogenous NO release were lost. Both treatments recovered these functions within 7days. These functions deteriorated after 116days of captopril but not losartan treatment. Inhibiting A2 formation during losartan treatment didn't alter BP or vascular recovery. The superior recovery of PDC by losartan over captopril was not produced by better BP, uremia or aldosterone control or elevated A2. PDC recovery was associated with improved PKC function and enhanced basal NO release. The re-establishment of PDC could reduce cerebrovascular over-perfusion and hematoma expansion after stroke.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Captopril/farmacologia
Circulação Cerebrovascular/efeitos dos fármacos
Hipertensão/complicações
Infarto da Artéria Cerebral Média/tratamento farmacológico
Losartan/farmacologia
Artéria Cerebral Média/efeitos dos fármacos
[Mh] Termos MeSH secundário: Aldosterona/sangue
Animais
Pressão Sanguínea/efeitos dos fármacos
Modelos Animais de Doenças
Combinação de Medicamentos
Ativação Enzimática
Hipertensão/sangue
Hipertensão/metabolismo
Infarto da Artéria Cerebral Média/sangue
Infarto da Artéria Cerebral Média/etiologia
Infarto da Artéria Cerebral Média/fisiopatologia
Artéria Cerebral Média/metabolismo
Artéria Cerebral Média/fisiopatologia
Óxido Nítrico/metabolismo
Proteína Quinase C/metabolismo
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Sistema Renina-Angiotensina/efeitos dos fármacos
Fatores de Tempo
Ureia/sangue
Ácido Úrico/sangue
Vasoconstrição/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Drug Combinations); 268B43MJ25 (Uric Acid); 31C4KY9ESH (Nitric Oxide); 4964P6T9RB (Aldosterone); 8W8T17847W (Urea); 9G64RSX1XD (Captopril); EC 2.7.11.13 (Protein Kinase C); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE


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[PMID]:28679681
[Au] Autor:Azevedo ER; Mak S; Floras JS; Parker JD
[Ad] Endereço:Division of Cardiology, Department of Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada; Lunenfeld-Tanenbaum Research Institute, University of Toronto, Toronto, Ontario, Canada; and Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:Acute effects of angiotensin-converting enzyme inhibition versus angiotensin II receptor blockade on cardiac sympathetic activity in patients with heart failure.
[So] Source:Am J Physiol Regul Integr Comp Physiol;313(4):R410-R417, 2017 Oct 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (ANG II) receptor antagonists in patients with heart failure secondary to reduced ejection fraction (HFrEF) are felt to result from prevention of the adverse effects of ANG II on systemic afterload and renal homeostasis. However, ANG II can activate the sympathetic nervous system, and part of the beneficial effects of ACE inhibitors and ANG II antagonists may result from their ability to inhibit such activation. We examined the acute effects of the ACE inhibitor captopril (25 mg, = 9) and the ANG II receptor antagonist losartan (50 mg, = 10) on hemodynamics as well as total body and cardiac norepinephrine spillover in patients with chronic HFrEF. Hemodynamic and neurochemical measurements were made at baseline and at 1, 2, and 4 h after oral dosing. Administration of both drugs caused significant reductions in systemic arterial, cardiac filling, and pulmonary artery pressures ( < 0.05 vs. baseline). There was no significant difference in the magnitude of those hemodynamic effects. Plasma concentrations of ANG II were significantly decreased by captopril and increased by losartan ( < 0.05 vs. baseline for both). Total body sympathetic activity increased in response to both captopril and losartan ( < 0.05 vs. baseline for both); however, there was no change in cardiac sympathetic activity in response to either drug. The results of the present study do not support the hypothesis that the acute inhibition of the renin-angiotensin system has sympathoinhibitory effects in patients with chronic HFrEF.
[Mh] Termos MeSH primário: Antagonistas de Receptores de Angiotensina/farmacologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Captopril/farmacologia
Insuficiência Cardíaca/tratamento farmacológico
Coração/efeitos dos fármacos
Losartan/farmacologia
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Idoso
Antagonistas de Receptores de Angiotensina/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Captopril/uso terapêutico
Feminino
Coração/fisiopatologia
Insuficiência Cardíaca/fisiopatologia
Hemodinâmica/efeitos dos fármacos
Hemodinâmica/fisiologia
Seres Humanos
Losartan/uso terapêutico
Masculino
Meia-Idade
Sistema Renina-Angiotensina/efeitos dos fármacos
Sistema Renina-Angiotensina/fisiologia
Sistema Nervoso Simpático/fisiopatologia
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 9G64RSX1XD (Captopril); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00095.2017


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[PMID]:28636634
[Au] Autor:Mitrega KA; Spalek AM; Nozynski J; Porc M; Stankiewicz M; Krzeminski TF
[Ad] Endereço:Silesian Centre for Heart Diseases, Zabrze, Poland.
[Ti] Título:Cardiomyopathy development protection after myocardial infarction in rats: Successful competition for major dihydropyridines' common metabolite against captopril.
[So] Source:PLoS One;12(6):e0179633, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During the last 25 years angiotensin-converting enzyme inhibitors spectacularly conquered the field of cardiovascular diseases therapy. Nevertheless, lack of new studies concerning side effects associated with their chronic administration seems to be rather confusing. In our previous research, we proved that the main furnidipines' metabolite (M-2) possess multiple cardioprotective actions. Currently, we compared effects of post-infarction long-term oral treatment with M-2 and captopril on hemodynamic parameters and "ischemic cardiomyopathy" development in rats. Myocardial infarction was evoked by permanent left anterior descending coronary artery occlusion for 35 days. Surviving rats were treated with captopril (2 × 25 mg/kg) or M-2 (4 mg/kg) from 6th- 35th day. At 35th day rats' hearts were tested on working heart setup, where following parameters were measured: heart rate, preload pressure, aortic systolic and diastolic pressures, aortic maximum rise and fall, aortic and coronary flow, myocardial oxygen consumption and oximetry in perfusate. Subsequently, heart tissue specimens were assessed during morphological estimation. Captopril caused significant heart rate increase and markedly diminished preload pressure in comparison to M-2. Both drugs evoked essential aortic pressure increase. Aortic flow was significantly decreased after M-2, whereas captopril increased this parameter in comparison to M-2. Both agents caused marked coronary flow increase. Morphologic examination in captopril revealed cardiomyopathic process in 70% of hearts, whereas in M-2 this value reached 30%. Neovascularization of post-infarcted myocardium was visible only after M-2 therapy. Concluding, M-2 presented itself as more attractive agent in long-term post-infarction treatment by preventing cardiomyopathy development, angiogenesis stimulation and preserving cardiac performance.
[Mh] Termos MeSH primário: Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Captopril/uso terapêutico
Cardiomiopatias/prevenção & controle
Di-Hidropiridinas/metabolismo
Infarto do Miocárdio/tratamento farmacológico
[Mh] Termos MeSH secundário: Administração Oral
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Biomarcadores/sangue
Pressão Sanguínea/efeitos dos fármacos
Captopril/farmacologia
Cardiomiopatias/etiologia
Di-Hidropiridinas/farmacologia
Di-Hidropiridinas/uso terapêutico
Modelos Animais de Doenças
Coração/fisiopatologia
Frequência Cardíaca/efeitos dos fármacos
Hemodinâmica/efeitos dos fármacos
Masculino
Infarto do Miocárdio/mortalidade
Infarto do Miocárdio/patologia
Miocárdio/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Biomarkers); 0 (Dihydropyridines); 9G64RSX1XD (Captopril)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179633


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[PMID]:28592038
[Au] Autor:Chen S; Zeng ZP; Song AL; Zhu L; Lu L; Tong AL; Shi C; Li HZ
[Ti] Título:[The application of captopril challenge test in the diagnosis of primary aldosteronism].
[So] Source:Zhonghua Nei Ke Za Zhi;56(6):402-408, 2017 Jun 01.
[Is] ISSN:0578-1426
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To evaluate the value of captopril challenge test (CCT) in the diagnosis of primary aldosteronism (PA). A total of 674 patients [(45.0±13.7) years, men 341, women 333] admitted to Peking Union Medical College Hospital from 2000 to 2015 were analyzed. Among them, 222 subjects were with essential hypertension (EH), 28 were with pheochromocytoma (PHEO), 246 were with idiopathic hyperaldosteronism (IHA) and 178 were with aldosterone producing adenoma (APA). All patients received CCT. 24 h urine sodium was measured in partial patients. Plasma renin activity (PRA), aldosterone (ALD) were detected. Compared with EH [PRA: before 0.5(0.2, 0.9) µg·L(-1)·h(-1,) after 0.8(0.4, 1.5) µg·L(-1)·h(-1;) ALD: before (393±122) pmol/L, after (360±97) pmol/L] and PHEO [PRA: before 0.3(0.1, 0.9) µg·L(-1)·h(-1,) after 0.4(0.1, 1.6) µg·L(-1)·h(-1;) ALD: before (396±108) pmol/L, after (374±114) pmol/L], lower levels of PRA and higher levels of ALD before and after CCT were observed in PA patients [PRA: before 0.1 (0.1, 0.2) µg·L(-1)·h(-1,) after 0.1 (0.1, 0.2) µg·L(-1)·h(-1;) ALD: before (468±216) pmol/L; after (457±199) pmol/L]. After CCT, the suppression rate of ALD [2.8% (-8.8%, 15.4%) vs 6.6% (-4.3%, 17.6%)] and increasing rate of PRA [0(0, 50%) vs 50%(0, 200%)] in PA patients were lower than those in EH patients. The ALD/PRA ratio (ARR) were higher in PA than that in EH or PHEO patients. In the EH subjects, ALD levels of seated posture were higher than those of recumbent posture both before and after receiving captopril, but with no changes in ARR after CCT. No significant differences in ALD and ARR (before and after receiving captopril) were observed between seated and recumbent position in the PA group. The ARR after CCT tended to decrease in EH subjects with elevated urine-sodium compared with those with normal urine-sodium. No changes could be viewed in ALD and PRA levels between normal urine-sodium and elevated urine-sodium groups among APA, IHA and EH patients either before or after CCT. Among patients with APA, the ALD levels before CCT and the ARR after CCT were lower in the patients with Angiotensionâ…¡(Angâ…¡) reactive than those without. A ROC curve analysis suggested that the optimal cutoff value was 46.2 (ALD unit: ng/dl; PRA unit: µg·L(-1)·h(-1)) for ARR after challenge in diagnosing PA, with the sensitivity of 88.7% and specificity of 84.8%. ARR after 25 mg captopril had high sensitivity and specificity in diagnosis of PA with the cutoff of 46.2. Seated CCT could replace recumbent CCT as a more confirmatory test. The PRA increasing rate should be taken into consideration when diagnosis of PA.
[Mh] Termos MeSH primário: Neoplasias das Glândulas Suprarrenais/sangue
Aldosterona/sangue
Hiperaldosteronismo/diagnóstico
Feocromocitoma/sangue
Renina/sangue
[Mh] Termos MeSH secundário: Neoplasias das Glândulas Suprarrenais/complicações
Adulto
Captopril
Feminino
Hospitalização
Hospitais
Seres Humanos
Hiperaldosteronismo/sangue
Hiperaldosteronismo/complicações
Hiperaldosteronismo/fisiopatologia
Hipertensão/diagnóstico
Hipertensão/etiologia
Hipertensão/fisiopatologia
Masculino
Meia-Idade
Feocromocitoma/complicações
Postura
Valor Preditivo dos Testes
Curva ROC
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
4964P6T9RB (Aldosterone); 9G64RSX1XD (Captopril); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170904
[Lr] Data última revisão:
170904
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0578-1426.2017.06.004


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[PMID]:28578650
[Au] Autor:Waheed H; Moin SF; Choudhary MI
[Ad] Endereço:Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, 75270-Karachi, Pakistan.
[Ti] Título:Snake Venom: From Deadly Toxins to Life-saving Therapeutics.
[So] Source:Curr Med Chem;24(17):1874-1891, 2017.
[Is] ISSN:1875-533X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Snakes are fascinating creatures and have been residents of this planet well before ancient humans dwelled the earth. Venomous snakes have been a figure of fear, and cause notable mortality throughout the world. The venom constitutes families of proteins and peptides with various isoforms that make it a cocktail of diverse molecules. These biomolecules are responsible for the disturbance in fundamental physiological systems of the envenomed victim, leading to morbidity which can lead to death if left untreated. Researchers have turned these life-threatening toxins into life-saving therapeutics via technological advancements. Since the development of captopril, the first drug that was derived from bradykininpotentiating peptide of Bothrops jararaca, to the disintegrins that have potent activity against certain types of cancers, snake venom components have shown great potential for the development of lead compounds for new drugs. There is a continuous development of new drugs from snake venom for coagulopathy and hemostasis to anti-cancer agents. In this review, we have focused on different snake venom proteins / peptides derived drugs that are in clinical use or in developmental stages till to date. Also, some commonly used snake venom derived diagnostic tools along with the recent updates in this exciting field are discussed.
[Mh] Termos MeSH primário: Venenos de Serpentes/química
[Mh] Termos MeSH secundário: Animais
Anticoagulantes/química
Anticoagulantes/metabolismo
Anticoagulantes/uso terapêutico
Batroxobina/química
Batroxobina/uso terapêutico
Coagulação Sanguínea/efeitos dos fármacos
Captopril/química
Captopril/uso terapêutico
Peptídeos/metabolismo
Peptídeos/farmacologia
Peptídeos/uso terapêutico
Venenos de Serpentes/metabolismo
Serpentes/metabolismo
Trombose/tratamento farmacológico
Trombose/patologia
Toxinas Biológicas/metabolismo
Toxinas Biológicas/farmacologia
Toxinas Biológicas/uso terapêutico
Tirosina/análogos & derivados
Tirosina/química
Tirosina/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticoagulants); 0 (Peptides); 0 (Snake Venoms); 0 (Toxins, Biological); 42HK56048U (Tyrosine); 9G64RSX1XD (Captopril); EC 3.4.21.- (Batroxobin); GGX234SI5H (tirofiban)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.2174/0929867324666170605091546


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[PMID]:28435253
[Au] Autor:Miyata S; Miyaji H; Kawasaki H; Yamamoto M; Nishida E; Takita H; Akasaka T; Ushijima N; Iwanaga T; Sugaya T
[Ad] Endereço:Department of Periodontology and Endodontology, Hokkaido University Graduate School of Dental Medicine, Kita-ku, Sapporo.
[Ti] Título:Antimicrobial photodynamic activity and cytocompatibility of Au (Capt) clusters photoexcited by blue LED light irradiation.
[So] Source:Int J Nanomedicine;12:2703-2716, 2017.
[Is] ISSN:1178-2013
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Antimicrobial photodynamic therapy (aPDT) has beneficial effects in dental treatment. We applied captopril-protected gold (Au (Capt) ) clusters as a novel photosensitizer for aPDT. Photoexcited Au clusters under light irradiation generated singlet oxygen ( O ). Accordingly, the antimicrobial and cytotoxic effects of Au (Capt) clusters under dental blue light-emitting diode (LED) irradiation were evaluated. O generation of Au (Capt) clusters under blue LED irradiation (420-460 nm) was detected by a methotrexate (MTX) probe. The antimicrobial effects of photoexcited Au clusters (0, 5, 50, and 500 µg/mL) on oral bacterial cells, such as , and , were assessed by morphological observations and bacterial growth experiments. Cytotoxicity testing of Au clusters and blue LED irradiation was then performed against NIH3T3 and MC3T3-E1 cells. In addition, the biological performance of Au clusters (500 µg/mL) was compared to an organic dye photosensitizer, methylene blue (MB; 10 and 100 µg/mL). We confirmed the O generation ability of Au (Capt) clusters through the fluorescence spectra of oxidized MTX. Successful application of photoexcited Au clusters to aPDT was demonstrated by dose-dependent decreases in the turbidity of oral bacterial cells. Morphological observation revealed that application of Au clusters stimulated destruction of bacterial cell walls and inhibited biofilm formation. Aggregation of Au clusters around bacterial cells was fluorescently observed. However, photoexcited Au clusters did not negatively affect the adhesion, spreading, and proliferation of mammalian cells, particularly at lower doses. In addition, application of Au clusters demonstrated significantly better cytocompatibility compared to MB. We found that a combination of Au (Capt) clusters and blue LED irradiation exhibited good antimicrobial effects through O generation and biosafe characteristics, which is desirable for aPDT in dentistry.
[Mh] Termos MeSH primário: Anti-Infecciosos/química
Anti-Infecciosos/farmacologia
Ouro/farmacologia
Fotoquimioterapia/métodos
Fármacos Fotossensibilizantes/farmacologia
[Mh] Termos MeSH secundário: Aggregatibacter actinomycetemcomitans/efeitos dos fármacos
Animais
Captopril/química
Captopril/farmacologia
Corantes
Ouro/química
Luz
Azul de Metileno/farmacologia
Camundongos
Células NIH 3T3/efeitos dos fármacos
Fármacos Fotossensibilizantes/química
Porphyromonas gingivalis/efeitos dos fármacos
Oxigênio Singlete/metabolismo
Streptococcus mutans/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Coloring Agents); 0 (Photosensitizing Agents); 17778-80-2 (Singlet Oxygen); 7440-57-5 (Gold); 9G64RSX1XD (Captopril); T42P99266K (Methylene Blue)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.2147/IJN.S131602


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[PMID]:28355350
[Au] Autor:Nunes AD; Souza AP; Macedo LM; Alves PH; Pedrino GR; Colugnati DB; Mendes EP; Santos RA; Castro CH
[Ad] Endereço:Departamento de Ciências Fisiológicas, Universidade Federal de Goiás, Goiânia, GO, Brasil.
[Ti] Título:Influence of antihypertensive drugs on aortic and coronary effects of Ang-(1-7) in pressure-overloaded rats.
[So] Source:Braz J Med Biol Res;50(4):e5520, 2017 Mar 23.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study investigated the influence of antihypertensive drugs, such as angiotensin-converting enzyme inhibitors (ACEIs), AT1 receptor blockers (ARBs), voltage-gated L-type calcium channel blockers, and mineralocorticoid receptor antagonists (MRAs), on the effects of angiotensin-(1-7) [Ang-(1-7)] on aorta and coronary arteries from pressure-overloaded rats. Pressure overload was induced by abdominal aortic banding (AB). To evaluate the role of antihypertensive drugs on the effect of Ang-(1-7), AB male Wistar rats weighing 250-300 g were treated with vehicle or low doses (5 mg·kg-1·day-1, gavage) of losartan, captopril, amlodipine, or spironolactone. Isolated aortic rings and isolated perfused hearts under constant flow were used to evaluate the effect of Ang-(1-7) in thoracic aorta and coronary arteries, respectively. Ang-(1-7) induced a significant relaxation in the aorta of sham animals, but this effect was reduced in the aortas of AB rats. Chronic treatments with losartan, captopril or amlodipine, but not with spironolactone, restored the Ang-(1-7)-induced aorta relaxation in AB rats. The coronary vasodilatation evoked by Ang-(1-7) in sham rats was blunted in hypertrophic rats. Only the treatment with losartan restored the coronary vasodilatory effect of Ang-(1-7) in AB rat hearts. These data support a beneficial vascular effect of an association of Ang-(1-7) and some antihypertensive drugs. Thus, this association may have potential as a new therapeutic strategy for cardiovascular diseases.
[Mh] Termos MeSH primário: Angiotensina I/farmacologia
Anti-Hipertensivos/farmacologia
Aorta Abdominal/efeitos dos fármacos
Vasos Coronários/efeitos dos fármacos
Fragmentos de Peptídeos/farmacologia
[Mh] Termos MeSH secundário: Anlodipino/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Pressão Sanguínea/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Captopril/farmacologia
Losartan/farmacologia
Masculino
Antagonistas de Receptores de Mineralocorticoides/farmacologia
Modelos Animais
Ratos Wistar
Reprodutibilidade dos Testes
Espironolactona/farmacologia
Fatores de Tempo
Vasoconstrição/efeitos dos fármacos
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Antihypertensive Agents); 0 (Calcium Channel Blockers); 0 (Mineralocorticoid Receptor Antagonists); 0 (Peptide Fragments); 1J444QC288 (Amlodipine); 27O7W4T232 (Spironolactone); 9041-90-1 (Angiotensin I); 9G64RSX1XD (Captopril); IJ3FUK8MOF (angiotensin I (1-7)); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170330
[St] Status:MEDLINE


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[PMID]:28260186
[Au] Autor:Omboni S; Malacco E; Napoli C; Modesti PA; Manolis A; Parati G; Agabiti-Rosei E; Borghi C
[Ad] Endereço:Clinical Research Unit, Italian Institute of Telemedicine, Varese, Italy. stefano.omboni@iitelemed.org.
[Ti] Título:Efficacy of Zofenopril vs. Irbesartan in Combination with a Thiazide Diuretic in Hypertensive Patients with Multiple Risk Factors not Controlled by a Previous Monotherapy: A Review of the Double-Blind, Randomized "Z" Studies.
[So] Source:Adv Ther;34(4):784-798, 2017 Apr.
[Is] ISSN:1865-8652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Combinations between an angiotensin converting enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) and hydrochlorothiazide (HCTZ) are among the recommended treatments for hypertensive patients uncontrolled by monotherapy. Four randomized, double-blind, parallel group studies with a similar design, including 1469 hypertensive patients uncontrolled by a previous monotherapy and with ≥1 cardiovascular risk factor, compared the efficacy of a combination of a sulfhydryl ACE inhibitor (zofenopril at 30 or 60 mg) or an ARB (irbesartan at 150 or 300 mg) plus HCTZ 12.5 mg. The extent of blood pressure (BP)-lowering was assessed in the office and over 24 h. Pleiotropic features of the treatments were evaluated by studying their effect on systemic inflammation, organ damage, arterial stiffness, and metabolic biochemical parameters. Both treatments similarly reduced office and ambulatory BPs after 18-24 weeks. In the ZODIAC study a larger reduction in high sensitivity C reactive protein (hs-CRP) was observed under zofenopril (-0.52 vs. +0.97 mg/dL under irbesartan, p = 0.001), suggesting a potential protective effect against the development of atherosclerosis. In the ZENITH study the rate of carotid plaque regression was significantly larger under zofenopril (32% vs. 16%; p = 0.047). In the diabetic patients of the ZAMES study, no adverse effects of treatments on blood glucose and lipids as well as an improvement of renal function were observed. In patients with isolated systolic hypertension of the ZEUS study, a slight and similar improvement in renal function and small reductions in pulse wave velocity (PWV), augmentation index (AI), and central systolic BP were documented with both treatments. Thus, the fixed combination of zofenopril and HCTZ may have a relevant place in the treatment of high-risk or monotherapy-treated uncontrolled hypertensive patients requiring a more prompt, intensive, and sustained BP reduction, in line with the recommendations of current guidelines.
[Mh] Termos MeSH primário: Anti-Hipertensivos/uso terapêutico
Compostos de Bifenilo/uso terapêutico
Captopril/análogos & derivados
Hidroclorotiazida/uso terapêutico
Hipertensão/tratamento farmacológico
Tetrazóis/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Antagonistas de Receptores de Angiotensina/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anti-Hipertensivos/administração & dosagem
Biomarcadores
Compostos de Bifenilo/administração & dosagem
Glicemia
Pressão Sanguínea/efeitos dos fármacos
Proteína C-Reativa/metabolismo
Captopril/administração & dosagem
Captopril/uso terapêutico
Diabetes Mellitus/epidemiologia
Método Duplo-Cego
Quimioterapia Combinada
Feminino
Seres Humanos
Hidroclorotiazida/administração & dosagem
Hipertensão/epidemiologia
Mediadores da Inflamação/metabolismo
Lipídeos/sangue
Masculino
Meia-Idade
Análise de Onda de Pulso
Ensaios Clínicos Controlados Aleatórios como Assunto
Fatores de Risco
Tetrazóis/administração & dosagem
Rigidez Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Antihypertensive Agents); 0 (Biomarkers); 0 (Biphenyl Compounds); 0 (Blood Glucose); 0 (Inflammation Mediators); 0 (Lipids); 0 (Tetrazoles); 0J48LPH2TH (Hydrochlorothiazide); 290ZY759PI (zofenopril); 9007-41-4 (C-Reactive Protein); 9G64RSX1XD (Captopril); J0E2756Z7N (irbesartan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:T
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE
[do] DOI:10.1007/s12325-017-0497-8


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[PMID]:28219104
[Au] Autor:Queiroz AC; Sousa JC; Silva ND; Tobaldini E; Ortega KC; de Oliveira EM; Brum PC; Montano N; Mion D; Tinucci T; de Moraes Forjaz CL
[Ad] Endereço:School of Physical Education and Sport, University of Sao Paulo, São Paulo, Brazil.
[Ti] Título:Captopril does not Potentiate Post-Exercise Hypotension: A Randomized Crossover Study.
[So] Source:Int J Sports Med;38(4):270-277, 2017 Apr.
[Is] ISSN:1439-3964
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:To evaluate whether captopril (3×50 mg/day) potentiates post-resistance exercise hypotension (PREH) in hypertensives (HT), 12 HT men received captopril and placebo for 4 weeks each in a double-blinded, randomized-crossover design. On each therapy, subjects underwent 2 sessions: Control (C - rest) and Resistance Exercise (RE - 7 exercises, 3 sets to moderate fatigue, 50% of 1 RM -repetition maximum). Measurements were taken before and after 30-60 min (Post1) and 7 h (Post2), and ambulatory blood pressure (BP) was monitored for 24 h. There were no differences in PREH characteristics and mechanisms between the placebo and captopril periods. At Post1, systolic/diastolic BP decreased significantly and similarly after RE with both therapies (Placebo=-13±2/-9±1 mmHg vs. Captopril=-12±2/-10±1 mmHg, P<0.05). RE reduced cardiac output in some subjects and systemic vascular resistance in others. Heart rate and cardiac sympathetic modulation increased, while stroke volume and baroreflex sensitivity decreased after RE (Placebo: +13±2 bpm, +21±5 nu, -11±5 ml, -4±2 ms/mmHg; Captopril: +13±2 bpm, +35±4 nu, 17±5 ml, -3±1 ms/mmHg, P<0.05). At Post2, all variables returned to pre-intervention values. Ambulatory BP was similar between the sessions. Thus, captopril did not potentiate the magnitude and duration of PREH in HT men, and it did not influence PREH mechanisms.
[Mh] Termos MeSH primário: Captopril/administração & dosagem
Hipertensão/fisiopatologia
Hipotensão Pós-Exercício/tratamento farmacológico
Treinamento de Resistência
[Mh] Termos MeSH secundário: Anti-Hipertensivos/administração & dosagem
Pressão Sanguínea
Estudos Cross-Over
Método Duplo-Cego
Frequência Cardíaca
Hemodinâmica
Seres Humanos
Masculino
Meia-Idade
Volume Sistólico
Resistência Vascular
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antihypertensive Agents); 9G64RSX1XD (Captopril)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170413
[Lr] Data última revisão:
170413
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170221
[St] Status:MEDLINE
[do] DOI:10.1055/s-0042-123044



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