Role of Renal Nerves, Angiotensin II, and Prostaglandins in the Antinatriuretic Response to Acute Hypercapnic Acidosis in the Dog

SUMMARY Although clinical studies suggest that chronic hypercapnic acidosis may be associated with renal sodium retention, little information is available on the effect of acute hypercapnic acidosis on renal sodium excretion. We, therefore, increased Pco2 from 23 to 74 nun Hg in anesthetized dogs and observed a marked antinatriuresis as absolute sodium excretion (235 to 60 juEq/min, P < 0.001) and fractional excretion of sodium (4.0 to 1.2%, P < 0.02) decreased significantly. This decrease in sodium excretion occurred independent of consistent changes in renal perfusion pressure, Po2, glomerular filtration rate, renal blood flow, extraction of p-aminohippuric acid, and filtration fraction. The antinatriuretic response to acute hypercapnic acidosis could be attenuated significantly by surgical renal denervation, intrarenal phenoxybenzamine, and by intrarenal infusion of l-sarcosine,8-glycine angiotensin II. Administration of 10 mg/kg indomethacin enhanced the antinatriuretic response to hypercapnic acidosis in denervated kidneys. These results suggest that renal a-adrenergic nerves and the renin angiotensin system result in an antinatriuretic effect during acute hypercapnic acidosis. Renal prostaglandins or related substances may serve to attenuate this antinatriuretic response. Circ Res 50: 294-300, 1982 SEVERAL clinical observations have suggeste