Influence of the Intrarenal Baroreceptor on Renin Release During Acute Respiratory Acidosis in Dog

The role of the renal vascular baroreceptor mechanism in the renin response elicited by acute respiratory acidosis was studied in 8 chloralose anesthetized dogs. Ventilation with 8% CO2 in air for 10 minutes (constant minute ventilation) resulted in a significant increase (P <0.01) in plasma renin activity (PRA) with a small, but insignificant, decrease in mean arterial pressure and increase in renal blood flow. The smooth muscle relaxant, papaverine, was infused into the renal artery (2 mg/min) to produced renal vasodilation and thus inhibit the renal vascular receptor for renin release. During intrarenal papaverine, the renin response to 8% CO2 inhalation was attenuated (P < 0.05) even though blood pressure fell (P < 0.01) by an average of 21 mmHg. The data indicated that the renin response during acute respiratory acidosis is papaverine sensitive and is mediated in part by the renal vascular baroreceptor mechanism.