Adrenergic control of the cardiovascular system in the turtle Trachemys scripta.
Freshwater turtles, Trachemys scripta, like all non-crocodilian reptiles, are able to shunt blood between the pulmonary and systemic circulations owing to their undivided ventricle. The prevailing hypothesis is that the ratio of pulmonary and systemic resistances is the primary determinant of cardiac shunting in turtles. In the present study, we have examined the adrenergic influences on vascular resistances in the pulmonary and systemic circulations and the associated effects on cardiac shunts in turtles. To achieve this objective, systemic blood flow and pressures and pulmonary blood flow and pressures were measured simultaneously in anaesthetised turtles during bolus injections of alpha- and beta-adrenergic agonists and antagonists. Total cardiac output, systemic vascular resistance, pulmonary vascular resistance, heart rate and cardiac stroke volume were derived from these measurements. Anaesthetised turtles showed cardiovascular characteristics that were similar to those of non-apnoeic non-anaesthetised turtles, because anaesthesia blocked the cholinergically mediated constriction of the pulmonary artery that is normally associated with apnoea. As a result, the anaesthetised turtles exhibited a large net left-to-right shunt, and the adrenergic responses could be observed without confounding changes resulting from apnoea. Potent alpha-adrenergic vasoconstriction and weaker beta-adrenergic vasodilation were discovered in the systemic circulation. Modest beta-adrenergic vasodilation and possible weak alpha-adrenergic vasodilation were discovered in the pulmonary circulation. This adrenergically mediated vasoactivity produced the largest range of cardiac shunts observed so far in turtles. Regression analysis revealed that 97% of the variability in the cardiac shunts could be accounted for by the ratio of the pulmonary and systemic resistances. Thus, we conclude that, independent of whether the pulmonary vascular resistance is modulated (as during apnoea) or the systemic resistance is modulated with adrenergic mechanisms (as shown here), the consequences on the cardiac shunt patterns are the same because they are determined primarily by the ratios of the pulmonary and systemic resistance.
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002302:Cardiac Output; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects; D006339:Heart Rate; D009638:Norepinephrine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000502:physiology*; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D013318:Stroke Volume; D014426:Turtles / Q000502:physiology*; D014655:Vascular Resistance
D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D009638:Norepinephrine