Pattern of sympathetic vasomotor activity in a model of hypertension induced by nitric oxide synthase blockade

Author(s)

Zambrano, I, Lysien ; Pontes, Roberto B. ^[1] ; Garcia, Michelle L. ^[1] ; Nishi, Erika E. ^[1] ; Nogueira, Fernando N. ^[2] ; Higa, Elisa M. S. ^[3] ; Cespedes, Juliana G. ^[4] ; Bergamaschi, Cassia T. ^[1] ; Campos, Ruy R. ^[1]

Affiliation

^[1] Zambrano, Lysien, I, Univ Fed Sao Paulo, Escola Paulista Med, Cardiovasc Div, Dept Physiol, Sao Paulo - Brazil

^[2] Univ Sao Paulo, Dept Biomat & Biol Oral, Fac Odontol, Sao Paulo - Brazil

^[3] Univ Fed Sao Paulo, Escola Paulista Med, Nephrol Div, Sao Paulo - Brazil

^[4] Univ Fed Sao Paulo, Inst Sci & Technol, Sao Jose Dos Campos - Brazil

• Document type: Journal article
• Source: PHYSIOLOGICAL REPORTS; v. 7, n. 14 JUL 2019.
• Web of Science Citations: 0

Abstract

We aimed to investigate the effects of nitric oxide (NO) synthesis inhibition by NO synthase inhibitor N-nitro-L-arginine-methyl ester (L-NAME) treatment on the sympathetic vasomotor nerve activity (SNA) on two sympathetic vasomotor nerves, the renal and splanchnic. NO plasma level and systemic oxidative stress were assessed. Hypertension was induced by L-NAME (20mg/kg per day, by gavage, for seven consecutive days) in male Wistar rats. At the end of the treatment, blood pressure, heart rate, arterial baroreflex sensitivity, renal SNA (rSNA), and splanchnic SNA (sSNA) were assessed in urethane anesthetized rats. L-NAME-treated rats presented increased blood pressure (152 +/- 2mmHg, n=17) compared to the control group (101 +/- 2 mm Hg, n=15). Both rSNA (147 +/- 10, n=15 vs. 114 +/- 5 Spikes/s, n=9) and sSNA (137 +/- 13, n=14 vs. 74 +/- 13 spikes/s, n=9) were significantly increased in the L-NAME-treated compared to the control group. A differential response on baroreflex sensitivity was found, with a significant reduction for rSNA but not for sSNA arterial baroreceptor sensitivity in L-NAME-treated rats. The adjusted regression model revealed that the reduction of systemic NO levels partially explains the variation in sSNA and blood pressure, but not rSNA. Taken together, our data show that hypertension induced by NO synthase blockade is characterized by increased SNA to the rSNA and sSNA. In addition, we found that the rats that had the greatest reduction in NO levels in plasma by L-NAME were those that developed higher blood pressure levels. The reduction in the NO level partially explains the variations in sSNA but not in rSNA. (AU)

• FAPESP's process: 18/02671-3 - Functional and molecular actions of renal nerve in experimental chronic renal failure
• Grantee: Cassia Marta de Toledo Bergamaschi
• Support type: Regular Research Grants
• FAPESP's process: 13/22522-9 - Role of renal sympathetic nerves on cardiovascular and renal alterations in renovascular hypertension
• Grantee: Ruy Ribeiro de Campos Junior
• Support type: Regular Research Grants
• FAPESP's process: 13/23741-6 - Evaluation of central mechanisms in the renorenal reflex and the role of afferent renal nerves in renovascular hypertension
• Grantee: Erika Emy Nishi
• Support type: Scholarships in Brazil - Post-Doctorate