Kidney function during common carotid artery occlusion in anaesthetized cats: influence of vagotomy, constant ventilation, blood pressure stabilization, and carotid body chemoreceptor inactivation.

The reactions of kidney function elicited by bilateral common carotid artery occlusion were studied in six groups of chloralosed cats in which the Nn. vagi, the breathing reaction, the increase of the mean systemic arterial blood pressure, and the carotid body chemoreceptors were excluded successively. Carotid occlusion in the control animals caused a rise of the mean systemic arterial blood pressure, hyperventilation, and an increase in renal sodium and water excretion, resulting from an inhibition of tubular reabsorption. Bilateral cervical vagotomy, relaxation and constant artificial ventilation only slightly modified this renal response. Inactivation of the carotid body chemoreceptors in vagotomized and constantly ventilated cats attenuated the natriuresis due to carotid occlusion regardless of the behaviour of the renal perfusion pressure. On the other hand, keeping the mean arterial blood pressure during carotid occlusion constant by the bleeding technique also reduced the natriuretic reaction. Cats with both inactivated carotid body chemoreceptors and constant renal perfusion pressure exhibited an antinatriuretic reaction during carotid clamping. From these data it is concluded that in narcotized cats the natriuretic response during carotid occlusion is the result of both a stimulation of the carotid body chemoreceptors and the rise of the renal perfusion pressure. In contrast, in dogs this so-called carotid-sinus-polyuria seems to be induced solely by the increase of the systemic arterial blood pressure. The findings additionally indicated that the arterial chemoreceptors may be involved in the physiological daily control of renal sodium excretion already at normal arterial oxygen tension under sea-level conditions.