Roles of renal sympathetic nerves on production of angiotensin II and its effect on renal circulation during acute respiratory acidosis

Roles of renal sympathetic nerves on production of angiotensin II (AT II) and the effects of AT II on the systemic hemodynamics and renal circulation were evaluated in six mongrel dogs during acute respiratory acidosis. After unilateral kidney was denervated, 14% carbon dioxide (CO_2) ws inhalated, after which Captoprill 10μg/kg was administered intravenously. Heart rate, mean aortic pressure, cardiac output, total systemic vascular resistance and left ventricular end-diastolic pressure were measured. For the parameters of renal circulation, renal blood flow (RBF) and renal vascular resistance (RVR) were measured both in the innervated and denervated kidneys. The AT II sampled in the renal veins were measured by radioimmunoassay. In the condition of severe respiratory aditodis, PH decreased from 7.32±0.05 to 6.91±0.05 and PaCO_2 increased from 38.6±3.3 to 110.2±9.9 mmHg. The AT increased both in the innervated (p＜0.01) and denervated kidneys (p＜0.01) compared with the cntrol values, and the increase of ATII in the innervated kidney was greater than that in the denervated kidney (p＜0.01). After Captopril was administered intravenously, similar tendency to increase in AT II was observed. Compared with the control values, RBF decreased (p＜0.01) and RVR increased (p＜0.05) during severe respiratory acidosis in the innervated kidney, whereas no significant changes in the paramaters of systemic hemodynamics and denervated renal circulation were observed. In conclusion, renal sympathetic nerves have a relationship to renal AT II processing, and AT II affects renal vascular systems only when renal sympathic nerves is normally preserved during severe respiratory acidosis.