Abstract
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.
