NERVE-MEDIATED ANTIDIURESIS AND ANTINATRIURESIS AFTER AIR-JET STRESS IS MODULATED BY ANGIOTENSIN-II

A putative interaction between angiotensin II (Ang II) and the sympath etic nervous system within the kidney has been reported. We tested the hypothesis in conscious rats that endogenous Ang II modulates the ren al effects of a stress-induced increase in sympathetic nerve activity. We recorded mean arterial blood pressure, heart rate, renal sympathet ic nerve activity, renal hemodynamics; urine volume, and urinary sodiu m content in conscious rats. We used the Ang II type 1 receptor blocke r ZD 7155 to inhibit the effects of endogenous Ang II. Ten minutes of air-jet stress increased renal sympathetic nerve activity by 98 +/- 4% (n = 6) without changing systemic hemodynamics. Air-jet stress reduce d urine volume (from 31 +/- 3 to 8 +/- 4 mu L/min per gram kidney weig ht, P < .05, n = 12) and sodium excretion (from 4.3 +/- 0.9 to 1.2 +/- 0.3 mu mol/min per gram kidney weight, P < .05, n = 12). After renal denervation, air-jet Stress had no effect on either parameter. Six mic rograms of the Ang II type 1 receptor inhibitor ZD 7155 blunted the de crease in urine volume and sodium excretion in response to air-jet str ess, although the increase in renal sympathetic nerve activity during air-jet stress and the presser response to exogenous Ang II were not a ffected. Glomerular filtration rate and renal plasma flow were also no t affected. Higher doses of 30 and 60 mu g ZD 7155 inhibited the press er response to exogenous Ang II and abolished the changes in urine vol ume and sodium excretion in response to air-jet stress. None of the ZD 7155 doses affected urinary sodium excretion permanently. Hence, the Ang II type 1 receptor antagonist ZD 7155 impaired or abolished the re nal nerve-mediated antinatriuresis and anitidiuresis in response to ai r-jet stress. We conclude that endogenous Ang II modulates the renal e ffects of centrally mediated changes of sympathetic nerve activity in conscious rats.