ACUTE-HYPOXIA STIMULATES RENIN SECRETION AND RENIN GENE-EXPRESSION IN-VIVO BUT NOT IN-VITRO

This study aimed at examining the influence of acute hypoxia on renin secretion and renin gene expression in the kidney. To this end, male S prague-Dawley rats were exposed to severe hypoxic stress (8% O-2) or t o carbon monoxide (0.1% CO) for 6 h, and plasma renin activity (PRA) a nd renal renin mRNA levels were determined. PRA values increased from 3 to 13 and 10 ng angiotensin I.h(-1).ml(-1), and renin mRNA levels in creased by 120 and 100% during hypoxia and CO, respectively. Lowering the Po-2 from 150 to 20 or 7 mmHg in the gas atmosphere of primary cul tures of renal juxtaglomerular cells had no influence on renin secreti on and renin gene expression after 6 and 20 h. Our findings thus sugge st that both arterial and venous hypoxia can be powerful stimulators o f renin secretion and renin gene expression in vivo. Because renal den ervation did not prevent stimulation of the renin system by hypoxia, t he effect could be indirectly mediated via the baroreceptor-macula den sa mechanism. Another potential mediator of the effect could be circul ating catecholamines, since we found that plasma norepinephrine increa sed from 0.7 to 1.5 and 2.4 ng/ml and plasma epinephrine increased fro m 0.3 to 1.4 and 2.7 ng/ml during hypoxia and CO inhalation, respectiv ely.