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AbstractUnderstanding the basis of vascular tonus regulation is fundamental to comprehending cardiovascular physiology. In the present study, we used the recently developed decerebrate rattlesnake preparation to investigate the role of nitric oxide (NO) in the control of vascular tonus in a squamate reptile. This preparation allowed multiple concomitant cardiovascular parameters to be monitored, while avoiding the deleterious effect of anesthetic drugs on autonomic modulation. We observed that both systemic and pulmonary circuits were clearly responsive to NO signaling. NO increased vascular conductance in the systemic and pulmonary systems. Vasodilation by NO of the systemic circulation was compensated by cardiovascular alterations involving venous return, cardiac output, and cardiac shunt adjustments. The cardiac shunt seemed to be actively used for hemodynamic adjustments via modulation of the pulmonary artery constriction. N(ω)-nitro-L-arginine methyl ester injection demonstrated that NO contributes to modulating resting vasodilation in the systemic circuit. In contrast, NO-mediated vasodilation did not have an important role in the pulmonary circulation in inactive decerebrated snakes at 25°C. These responses vary importantly from those described for anesthetized snakes.

In humans, physical exercise imposes narrower limits for the heart rate (f H ) response of the baroreflex, and vascular modulation becomes largely responsible for arterial pressure regulation. In undisturbed reptiles, the baroreflex-related f H alterations at the operating point (G op ) decreases at elevated body temperatures (T b ) and the vascular regulation changes accordingly. We investigated how the baroreflex of rattlesnakes, Crotalus durissus, is regulated during an activity at different T b , expecting that activity would reduce the capacity of the cardiac baroreflex neural pathway to buffer arterial pressure fluctuations while being compensated by the vascular neural pathway regulation. Snakes were catheterized for blood pressure assessment at three different T b : 15, 20 and 30 °C. Data were collected before and after activity at each T b . Baroreflex gain (G op ) was assessed with the sequence method; the vascular limb, with the time constant of pressure decay (τ), using the two-element Windkessel equation. Both G op and τ reduced when T b increased. Activity also reduced G op and τ in all T b . The relationship between τ and pulse interval (τ/PI) was unaffected by the temperature at resting snakes, albeit it reduced after activity at 20 °C and 30 °C. The unchanged τ/PI and normalized G op at different T b indicated those variables are actively adjusted to work at different f H and pressure conditions at rest. Our data suggest that during activity, the baroreflex-related f H response is attenuated and hypertension is buffered by a disproportional increase in the rate which pressure decays during diastole. This compensation seems especially important at higher T b where G op is already low., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)