ROLE OF THE INTERSTITIAL HYDROSTATIC-PRES SURE AND ANGIOTENSIN-II ON THE RENAL RESPONSE TO EXTRACELLULAR VOLUME EXPANSION

Natriuresis induced by extracellular volume expansion (ECVE) is accomp anied by a decrease in renin release and by an increase of renal inter stitial hydrostatic pressure (RIHP). The main purpose of the present s tudy was to determine in anesthetized dogs if small increments in RHIP contribute to the renal excretory response to an ECVE. We also sought to evaluate the relative roles of intrarenal angiotensin II (Ang II) changes in mediating natriuresis and increases in RIHP induced by ECVE . Volume expansion (5 % body wt in 45 min) was induced with isotonic s aline. In the control group (n = 5), it was found that ECVE induced si gnificant incremelnts (p < 0,05) in natriuresis and RHIP that were sim ilar in both kidneys. In a second experimental group (n = 6), intraren al Ang II levels were maintained in the right kidney throughout the ex periment by simultaneously infusing captopril (0,8, mu g/kg/min) and A ng II (1 ng/kg/min) into the right renal artery. In response to ECVE, natriuresis was significantly greater in the left (421 +/- 59 ,mu eq/m in) than in the right kidney (248 +/- 45 ,mu eq/min). The reduced natr iuretic response to ECVE in the right kidney was accompanied by an inc rement in RHIP (3,8 +/- 1,5 mmHg) that was significantly smaller (p < 0,05) than that found in the left kidney (8,0 +/- 2, 1 mmHg). In the t hird experimental group (n = 6), intrarenal Ang II levels were maintai ned in the right kidney during ECVE, and a decapsulation of the renal cortex was also performed in the right kidney to prevent the ECVE-indu ced increment in RHIP. The increment in natriuresis induced by the ECV E in this group was also greater (p < 0,05) in the left (422 +/- 55 mu eq/min) than in the right (231 +/- 30 mu eq/min) kidney where Ang II levels were maintained constant throughout the experiment. The antinat riuretic effect of Ang II in this group was similar to that found in g roup 2 despite the fact that RHIP did not increase in the right kidney and increased significantly (p < 0,05) in the left kidney (8,3 +/- 7, 2 mmHg). In summary the results of the present study suggest that intr arenal Ang II levels play an important role in mediating the ECVE-indu ced increments in natriuresis and RHIP. Furthermore, these results ind icate that small increments in RHIP do not contribute to the renal exc retory response to an ECVE.