AJP - Renal Physiology, Vol 259, Issue 3 466-F473, Copyright © 1990 by American Physiological Society
Neurogenic control of pressure natriuresis in conscious dogs
H. Ehmke, P. B. Persson, M. Seyfarth and H. R. Kirchheim
I. Physiologisches Institut der Universitat Heidelberg, Federal Republic of Germany.
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.
