Endogenous production of nitric oxide via eNOS contributes to the vasodilator effect of sodium nitroprusside: studies in normotensive and hypertensive rats (SHR)

• Grant number: 18/02291-6
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): July 01, 2018
• Effective date (End): June 30, 2019
• Field of knowledge: Biological Sciences - Pharmacology - Cardiorenal Pharmacology
• Principal Investigator: Lusiane Maria Bendhack
• Grantee: Matheus Henrique da Silva
• Host Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Nitric oxide (NO) plays a pivotal role on the vascular tone control. NO is synthesized on the endothelial cells by the endothelial nitric oxide synthase (eNOS). Spontaneously hypertensive rat (SHR) vessels are characterized by endothelial dysfunction that leads to decreased NO bioavailability able to induce vasodilatation. Sodium nitroprusside (SNP) is an NO donor that is a pharmacological tool to release NO in the endothelial and vascular smooth muscle cells. Our hypothesis in the present work is that the SNP can positively modulate the eNOS activity. Thus, the SNP vasodilator effect would be potentiated in normotensive rat aorta. However, in SHR aortas the cellular mechanisms could be different. Therefore, this study aims to evaluate if the endothelium-dependent relaxation is modulated by SNP, in normotensive and SHR rat aortas. With this purpose, we will perform experiments on vascular reactivity studies in isolated aortas from normotensive rats and SHR. Aortic rings will be stimulated with increasing concentrations of SNP in the absence (control) and after incubation with the NOS inhibitor (L-NAME), its cofactor (BH4), and its substrate (L-arginine). (AU)