Nitric oxide (NO) plays a role in thermogenesis but does not mediate immune-to-brain febrigenic signaling in rats. There are suggestions of a different situation in birds, but the underlying evidence is not compelling. The present study was designed to clarify this matter in 5-day-old chicks challenged with a low or high dose of bacterial LPS. The lower LPS dose (2 μg/kg im) induced fever at 3-5 h postinjection, whereas 100 μg/kg im decreased core body temperature (Tc) (at 1 h) followed by fever (at 4 or 5 h). Plasma nitrate levels increased 4 h after LPS injection, but they were not correlated with the magnitude of fever. The NO synthase inhibitor (N(G)-nitro-l-arginine methyl ester, l-NAME; 50 mg/kg im) attenuated the fever induced by either dose of LPS and enhanced the magnitude of the Tc reduction induced by the high dose in chicks at 31-32°C. These effects were associated with suppression of metabolic rate, at least in the case of the high LPS dose. Conversely, the effects of l-NAME on Tc disappeared in chicks maintained at 35-36°C, suggesting that febrigenic signaling was essentially unaffected. Accordingly, the LPS-induced rise in the brain level of PGE2 was not affected by l-NAME. Moreover, l-NAME augmented LPS-induced huddling, which is indicative of compensatory mechanisms to run fever in the face of attenuated thermogenesis. Therefore, as in rats, systemic inhibition of NO synthesis attenuates LPS-induced fever in chicks by affecting thermoeffector activity and not by interfering with immune-to-brain signaling. This may constitute a conserved effect of NO in endotherms.
Baroreflex regulation of blood pressure is important for maintaining appropriate tissue perfusion. Although temperature affects heart rate ( f H ) reflex regulation in some reptiles and toads, no data are available on the influence of temperature-independent metabolic states on baroreflex. The South American tegu lizard Salvator merianae exhibits a clear seasonal cycle of activity decreasing f H along with winter metabolic downregulation, independent of body temperature. Through pharmacological interventions ( phenylephrine and sodium nitroprusside), the baroreflex control of f H was studied at ∼25°C in spring-summer-and winter-acclimated tegus. In winter lizards, resting and minimum f H were lower than in spring-summer animals (respectively, 13.3±0.82 versus 10.3±0.81 and 11.2±0.65 versus 7.97±0.88 beats min −1
Tegu lizards have hearts with a ventricule anatomically and functionally undivided. Thus, blood pressures are equal in the systemic and pulmonary circulations leading to a blood flow distribution dependent on their relative vascular resistances. There is evidence for the baroreflex control in some species of reptiles, but no conclusive data exist for tegus. The present study aimed to verify the presence of a functional baroreflex in the tegu lizard, Tupinambis merianae, during winter (hibernation; June‐August) and spring (activity; October‐December). Arterial blood pressure (ABP) and heart rate (HR) were determined after systemic injections of sodium nitroprusside (SNP; 2.5, 5, 10, 25 μg/kg) and phenylephrine (PE; 5, 10, 25, 50 μg/kg). Experiments were conducted at 24–27oC in both seasons to eliminate temperature effect on ABP and HR. Basal ABP and HR were, respectively: 35.5 ± 1.3 mmHg and 10 ± 1.5 bpm (winter) and 34.7 ± 1.4 mmHg and 13.3 ± 0.7 bpm (spring). All doses of SNP caused significant increases in ABP with respective decreases in HR in both seasons. PE induced a dose dependent increase in ABP, a response that was more prominent during spring, but did not affect HR regardless season. The results indicate the presence of a hypotensive baroreflex in T. merianae during winter and spring. The lack of reflex response of HR to the PE injections remains to be clarified. Supported by FAPESP, CNPq. INCT Fisiologia Comparada.
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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