Vasoconstrictor Agents
Mostrando 25-29 de 29 artigos, teses e dissertações.
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25. Endothelium-dependent contractions and endothelial dysfunction in human hypertension
The endothelium is a crucial regulator of vascular physiology, producing in healthy conditions several substances with a potent antiatherosclerotic properties. Accordingly, the presence of endothelial dysfunction is associated with subclinical atherosclerosis and with an increased future risk of cardiovascular events. A large body of evidence supports the fu
Blackwell Publishing Ltd.
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26. Renin-Angiotensin System Inhibition in Conscious Sodium-Depleted Dogs: EFFECTS ON SYSTEMIC AND CORONARY HEMODYNAMICS
The role of the renin-angiotensin system in the regulation of the systemic and coronary circulations during sodium depletion was studied in conscious normotensive dogs by i.v. administration of teprotide (0.5 mg/kg), an angiotensin-converting enzyme inhibitor, and saralasin (0.05-5 μg/kg per min), an angiotensin-receptor antagonist. Sodium depletion was pro
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27. Dissociation of the antimicrobial activity of bacitracin USP from its renovascular effects.
Bacitracin is a nephrotoxic antibiotic that has recently been shown to induce contractile effects in aortas isolated from rabbits by stimulating receptors for 5-hydroxytryptamine (5-HT). The possible renovascular actions of this antibiotic were investigated. Bacitracin USP increased the vascular resistance in a concentration-dependent manner (9 to 175 microg
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28. Vascular hyporeactivity to vasoconstrictor agents and hemodynamic decompensation in hemorrhagic shock is mediated by nitric oxide.
This study investigates the role of nitric oxide (NO) and the induction of a calcium-independent NO synthase (NOS) in development of vascular hyporeactivity to norepinephrine (NE) and vascular decompensation associated with hemorrhagic shock (HS) in the anesthetized rat. HS for 120 min caused a time-dependent reduction of the pressor responses to NE. This hy
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29. Beneficial effects and improved survival in rodent models of septic shock with S-methylisothiourea sulfate, a potent and selective inhibitor of inducible nitric oxide synthase.
Enhanced formation of nitric oxide (NO) by both the constitutive and the inducible isoforms of NO synthase (NOS) has been implicated in the pathophysiology of a variety of diseases, including circulatory shock. Non-isoform-selective inhibition of NO formation, however, may lead to side effects by inhibiting the constitutive isoform of NOS and, thus, the vari