| A series of experiments were conducted to determine if central administration of angiotensin-II (ANG-II) acts on the anteroventral third ventricle to alter renal renin secretion rate and norepinephrine (NE) secretion rate from the neurally intact but vascularly isolated kidney. The results indicate that central ANG-II administration increases renal perfusate NE concentration and renal NE secretion rate during a constant flow (0.6 ul/min) or constant pressure (100 mmHg) perfusion in control animals but not in rats with lesions of the A3V. Furthermore, central ANG-II administration increases renal vascular resistance as determined by reductions in perfusate flow rate at 100 mmHg constant pressure. On the other hand, central ANG-II administration increases perfusate renin concentration while renin secretion rate is decreased secondary to decreases in renal perfusate flow rate.;In a final set of perfusion studies, kidneys were perfused with ADH following central ANG-II administration. Perfusion with ADH blocked the effects of central ANG-II administration on renin secretion rate while norepinephrine secretion rate is slightly decreased.;These results indicate that Angiotensin-II acts centrally on the A3V nuclei to modulate renal renin secretion rate, norepinephrine secretion rate and renal vascular resistance. Furthermore, ADH seems to act directly on the kidney to decrease renin secretion rate and norepinephrine secretion rate.;However, when increases in renal vascular resistance are blocked by perfusion with a media containing hydralazine or papaverine (which act directly on smooth muscle and do not antagonize sympathetic activity), central ANG-II administration does cause an increase in renin secretion rate. Furthermore, perfusion with a lidocaine containing media or surgical denervation of the kidney blocks the effects of central ANG-II administration on renin secretion rate, norepinephrine secretion rate and renal vascular resistance. |
