Acute hypoxia stimulates renin secretion and renin gene expression
in vivo but not in vitro.
Ritthaler, Theresia, Karin Schricker, Frieder Kees, Bernhard
Kr[umlaut]amer, Armin Kurtz .
Institut f[umlaut]ur Physiologie, Institut f[umlaut]ur
Pharmakologie and Medizinische Klinik und Poliklinik II der
Universit[umlaut]at Regensburg, Germany
APStracts 3:0397R, 1996.
This study aimed to examine the influence of acute hypoxia on renin
secretion and renin gene expression in the kidney. To this end male
Sprague-Dawley rats were exposed to severe hypoxic stress (8%O2) or
to carbon monoxide (0.1% CO) for 6 hours and plasma renin activity
(PRA) and renal renin m-RNA levels were determined. PRA values
increased from 3 to 13 and to 10 ng ANGI/h x ml and renin m-RNA
levels increased by 120% and by 100% during hypoxia and CO,
respectively. Lowering the oxygen tension from 150 mmHg to 20 or to 7
mmHg in the gas athmosphere of primary cultures of renal
juxtaglomerular cells had no influence on renin secretion and renin
gene expression after 6 and after 20 hours. Our findings thus suggest
that both arterial and venous hypoxia can be powerful stimulators of
renin secretion and renin gene expression in vivo. Since renal
denervation did not prevent the stimulation of the renin system by
hypoxia the effect could be indirectly mediated via the
baroreceptor/macula densa mechanism. Another potential mediator of
the effect could be circulating catecholamines, since we found that
plasma noradrenaline increased from 0.7 to 1.5 and to 2.4 ng/ml and
plasma adrenaline increased from 0.3 to 1.4 and to 2.7 ng/ml during
hypoxia and CO-inhalation, respectively.
Received 11 December 1995; accepted in final form 1 October 1996.
APS Manuscript Number R783-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996