PRESSURE INDEPENDENCE OF RENIN RELEASE BY ISOLATED KIDNEYS OF LYON HYPERTENSIVE RATS

In the present work the influence of perfusion pressure on renal functions and renin release was studied before and after the blockade of thromboxane A2/prostaglandin H-2 (TXA2/PGH2) receptors using isolated kidneys from 7-week-old genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) rats of the Lyon strain. Kidneys were single pass perfused with Krebs-Henseleit solution with a gelatine derivative (Polygeline) added as an oncotic agent. A servocontrolled system stabilized the renal perfusion pressure (RPP) at any chosen (+/-1 mm Hg) level. In baseline conditions (RPP, 90 mm Hg), LH (n=7) kidneys differed from LN (n=6) and LL (n=8) controls by increased vascular resistance, decreased glomerular filtration rate, and natriuresis. The LH kidney responses to stepwise changes in RPP (between 60 and 170 mm Hg) differed from those of LN and LL rats by a significantly lower perfusion flow, glomerular filtration rate, and natriuresis. Above all, the reduction in RPP, which induced a marked and highly reproducible renin release in LN and LL kidneys, was devoid of effects in LH kidneys. The blockade of TXA2/PGH2 receptors by AH23848 (4 x 10(-6) M) did not change the baseline (RPP, 90 mm Hg) functions of kidneys of the three strains. During changes in RPP, the responses of LN and LL kidneys were not modified, whereas LH kidneys exhibited significant increases in both glomerular filtration rate and natriuresis. Finally, AH23848 significantly decreased the renin release by kidneys of the three strains. It is concluded that renin release of LH isolated kidneys is independent of the perfusion pressure and that renal TXA2/PGH2 receptor activation participates in the renin release and in the altered functions exhibited by kidneys of LH rats.