Kidney function during arterial chemoreceptor stimulation. I. Influence of unilateral renal nerve section, bilateral cervical vagotomy, constant artificial ventilation, and carotid body chemoreceptor inactivation.

The reactions of renal hemodynamics and excretory function elicited by perfusion of the vascularly isolated carotid bodies with venous blood were studied in four groups of chloralosed cats in which the Nn. vagi, the breathing reactions, and the carotid body chemoreceptors were excluded successively. The kidney function was determined using clearance-techniques in both the innervated right and denervated left kidneys. In the animals with intact carotid chemoreceptors perfusion of the carotid bifurcations with venous blood caused a weak (4-6 mm Hg on the average) and transient increase of the mean systemic arterial blood pressure as well as a vasoconstriction and a fall of the blood flow and glomerular filtration rate in the innervated kidneys. In the spontaneously breathing animals carotid body chemoreceptor stimulation effected a rise of fractional sodium excretion only in the denervated kidneys whereas the relaxed and constantly ventilated cats showed a natriuretic response both at the innervated and denervated side. The reactions of renal excretory function did not correlate with those of renal hemodynamics. Vagotomy, relaxation, and constant artificial ventilation failed to abolish the responses elicited by stimulation of the chemoreceptors. Inactivation of the carotid body chemoreceptors by injecting acetic acid into the vascularly isolated carotid sinuses prevented both the hemodynamic and tubular reactions due to hypoxic-hypercapnic perfusion of the carotid bodies. The findings suggest that the arterial chemoreceptors control kidney function by specific reflex mechanisms. The influence of the carotid body chemoreceptors on kidney vasculature is mediated by the efferent renal nerves, whereas the control of renal tubular sodium reabsorption requires hormone action.