Role of brain nitric oxide in cardiovascular control of frogs

Abstract

The aim of the present study was to determine if nitric oxide (NO) acting on the brain of frogs presents an inhibitory effect on arterial blood pressure (ABP) and heart rate (HR) by reducing the sympathetic activity dependent on α and β adrenergic receptors. Thus, body temperature and ABP was measured by a telemetry device implanted into the abdominal cavity of american bullfrogs (250–350 g BW), with the catheter of the device inserted into the left aortic arch for ABP measurements. A guide cannula was implanted into brain lateral ventricle for injections of L‐NMMA (non selective NO synthase inhibitor) or mCSF (mock cerebrospinal fluid). A catheter was inserted into the femoral vein for injection of adrenergic antagonists (prazosin: α1; sotalol: β) and agonists (phenylephrine: α1; isoproterenol: β) or Ringer solution. Animals (n= 6) were maintained at 25oC during experiments. L‐NMMA increased (P< 0.05) ABP by 7.5±1.3 mmHg compared to mCSF (−0.5±0.7 mmHg) and did not change HR (delta HR: −1.37±1.8 bpm and −0.9±0.6 bpm, L‐NMMA and mCSF respectively). The pre‐treatment with prazosin, but not with sotalol, attenuated the hypertensive effect of L‐NMMA. The effectiveness of the α and β adrenergic antagonists was confirmed by the blockade of the respective adrenergic agonists. We conclude that NO seems to act on the brain of frogs as a hypotensive agent via a mechanism dependent on α, but not β, adrenergic receptors in the periphery.Supported by FAPESP and CNPq.