Mechanism of Incresed Renin Secretion during Acute Respiratory Acidosis

Previously, Fujii, H. et al. in our laboratory reported that plasma renin activity (PRA) increased during acute respiratory acidosis in dogs, and that the hypercapnic renin secretory response was attenuated with intrarenal papaverine infusion, but not inhibited completely. Papaverine, a vascular smooth muscle relaxant, is known to dilate the renal arterioles sufficiently to block the proposed renal vascular receptor component of the renin response to CO_2 inhalation. So, it was concluded that the renin response during acute respiratory acidosis was papaverine sensitive and was mediated in part by the renal vascular receptor. Since renin secretion is regulated by some mechanisms, including the renal vascular baroreceptor, the macula densa mechanism, the renal sympathetic nerves, circulating catecholamine and other factors, these factors may affect the renin secretion during acute respiratory acidosis. In the present study, effects of intrarenal papaverine infusion were examined during acute respiratory acidosis in dogs with a denervated nonfiltering kidney in which the renal sympathetic nerves and the macula densa mechanism were nonfunctional. This experimental model permits an observation of the role of the intrarenal baroreceptor, the macula densa mechanism and the renal sympathetic nerves during acute respiratory acidosis. The hypercapnic renin response was completely inhibited by intrarenal papaverine infusion in dogs with a denervated nonfiltering kidney. These results indicate that the hypercapnic renin response during acute respiratory acidosis is multifactorial and that the major factors which affect the renin secretion during acute respiratory acidosis are intrarenal baroreceptor, macula densa mechanism and the renal sympathetic nerves.