Abstract

The aim of the present study was to determine if nitric oxide (NO) acting on the brain of the tegu lizard Tupinambis merianae presents an inhibitory effect on arterial blood pressure (ABP) and heart rate (HR) by reducing the sympathetic activity dependent on α adrenergic receptors. 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 artery for ABP record and another one in the femoral vein for injections of α1‐adrenergic antagonist (prazosin) and agonist (phenylephrine) or saline. Experiments were conducted during spring (activity) and winter (hibernation) at 24–27°C to abolish temperature effect on ABP and HR. Basal ABP (mmHg) and HR (bpm) were, respectively: 35.2 ± 3.2 and 10.4 ± 1.5 (winter); 31.6 ± 1.5 and 11.8 ± 1.0 (spring). No seasonal variation of the basal values was observed. L‐NMMA increased ABP and HR in both seasons (P< 0.05), an effect that was more prominent during spring. The pre‐treatment with prazosin inhibited the hypertensive and taquicardic effects of L‐NMMA in both seasons. The effectiveness of prazosin was confirmed by the blockade of phenylephrine effects. We conclude that NO seems to act on the brain of tegus as a hypotensive agent via a mechanism dependent on α adrenergic receptors in the periphery. Supported by FAPESP and CNPq.

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