KIDNEY-FUNCTION DURING ARTERIAL CHEMORECEPTOR STIMULATION .2. SUPPRESSION OF PLASMA-ALDOSTERONE CONCENTRATION DUE TO HYPOXIC-HYPERCAPNIC PERFUSION OF THE CAROTID-BODIES IN ANESTHETIZED CATS

  • 1 January 1985
    • journal article
    • research article
    • Vol. 44  (5) , 711-722
Abstract
The reactions of the mean systemic arterial blood pressure, kidney function (clearance technique) and plasma aldosterone concentration (radioimmunoassay) elicited by perfusion of the vascularly isolated carotid bodies with venous blood were studied in two series of chloralosed, vagotomized, relaxed, and constantly ventilated cats undergoing saline diuresis. In one group of animals the carotid body chemoreceptors were left intact; in the other one, they were abolished by injecting acetic acid into the glomera carotici. In the cats with intact chemoreceptors perfusion of the carotid bodies with venous blood immediately caused a small and transient increase of the blood pressure, whereas renal plasma flow tended to fall despite continuous chemoreceptor stimulation. Renal fractional sodium excretion already increased in the first 25 min of chemoreceptor stimulation, whereas plasma aldosterone concentration showed a significant decrease only after 45 min of venous perfusion of the glomera carotici. Plasma electrolytes changed only little at that time. No clear relationships between the responses of plasma aldosterone and those of the other parameters measured could be obtained. On subsequent perfusion of the carotid bodies with arterial blood plasma aldosterone returned to the values determined before chemoreceptor stimulation. Inactivation of the carotid body chemoreceptors per se already enhanced plasma aldosterone concentration. Perfusion of the glomera carotici with venous blood in the cats with abolished chemoreceptors did not suppress plasma aldosterone content. The data show that plasma aldosterone changes are not involved in the development of the initial phase (first hour) of the inhibition of renal tubular sodium reabsorption provoked by arterial chemoreceptor stimulation, but during long-lasting chemoreceptor stimulation they might contribute to the maintenance of this type of natriuresis. Furthermore the experiments suggest that the decrease of plasma aldosterone repeatedly observed during exposure of mammals to acute hypoxic hypoxia is possibly the reflex result of the stimulation of the arterial chemoreceptors.