Bradykinin may be involved in neuropeptide y-induced diuresis,
natriuresis and calciuresis.
Bischoff, Angela, Wolfgang Rascher, and Martin C. Michel .
Department of Medicine, University of Essen, 45122 Essen, Germany,
and Department of Pediatrics, University of Giessen, 35385 Giessen,
Germany
APStracts 5:0120F, 1998.
Neuropeptide Y (NPY) can cause diuresis, natriuresis and calciuresis
in rats independent of the pressure natriuresis mechanism
(Pfl[umlaut]ugers Arch. Eur. J. Physiol. 435: 443-453, 1998). Since
this is seen upon systemic but not intrarenal NPY infusion, we have
investigated the possible mediator of tubular NPY effects in
anaesthetized rats. In the present study infusion of NPY (2
_g/kg/min) enhanced renovascular resistance by ( 8 mm Hg/(ml/min) and
urine and sodium excretion by ( 450 _l/15 min and ( 60-85 _mol/15
min, respectively. Acute renal denervation did not alter renovascular
or tubular NPY effects, indicating that a neuronally released
mediator is not involved. Treatment with the angiotensin II receptor
antagonist, losartan, prevented the decline of the renovascular
response with time but did not modify tubular NPY effects. The
bradykinin B2 receptor antagonist, icatibant, accelerated the decline
of the renovascular NPY effects with time; concomitantly it
attenuated NPY-induced diuresis and natriuresis and abolished NPY
-induced calciuresis. The converting enzyme inhibitor, ramiprilat,
prevented the decline of the renovascular response with time;
concomitantly it magnified the NPY-induced diuresis, natriuresis and
calciuresis. We conclude that bradykinin may be involved in NPY
-induced diuresis, natriuresis and in particular calciuresis.
Received 9 March 1998; accepted in final form 2 June 1998.
APS Manuscript Number F60-8.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 30 July 1998