Neurogenic control of pressure natriuresis in conscious dogs.
In this study we investigated the interaction of the sympathetic nervous system with renal perfusion pressure (RPP) in the short-term control of sodium excretion (UNa V). Pressure natriuresis curves (PNCs) were determined in 13 conscious dogs on a normal-salt diet during control conditions, bilateral common carotid occlusion (CCO), CCO combined with an intrarenal prazosin infusion, and during an intrarenal methoxamine infusion. RPP was reduced in controlled steps by inflation of a cuff placed around the renal artery. For controls, a reduction in RPP resulted in a strong decrease in urine output and UNaV. In all dogs, the PNC was closely related to individual resting blood pressure; UNaV fell to less than 50% of control (10-20 mmHg below resting blood pressure). A baroreflex activation of the sympathetic nervous system by CCO shifted PNC to the right by 10-15 mmHg (n = 8). Sensitivity of pressure natriuresis was not affected by CCO. The shift was blocked when the selective alpha 1-adrenoceptor antagonist prazosin was infused intrarenally during CCO (n = 9). Without CCO, prazosin had no effects on urine flow rate or UNaV at the control RPP. Similar to CCO, intrarenal infusion of the selective alpha 1-adrenoceptor agonist methoxamine shifted PNC to the right by 15-20 mmHg (n = 4). Neither renal blood flow nor glomerular filtration rate was significantly different between control and any experimental condition. These results indicate that the sympathetic nervous system regulates UNaV by shifting the PNC through intrarenal alpha 1-adrenoceptors without altering the sensitivity of pressure natriuresis.