AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 3 524-R532, Copyright © 1993 by American Physiological Society
Mechanisms for the diuresis of acute cold exposure: role for vasopressin?
D. E. Allen and M. Gellai
School of Life and Health Sciences, University of Delaware, Newark 19716.
The hypothesis that inhibition of vasopressin (VP) secretion initiates
cold-induced diuresis was tested in six Brattleboro homozygous (diabetes
insipidus, DI) rats exposed to 60 min at 5 degrees C. For 9-14 days before
cold exposure (CE) the rats were treated with VP (750 pg.kg-1.min-1)
subcutaneously via osmotic minipumps. Eight vehicle-treated Long-Evans (LE)
rats characterized the response to acute exposure at 5 degrees C.
Additional groups of six to eight LE and six DI rats were infused with VP
(30-90 pg.kg-1.min-1 iv) on the day of CE. The DI rats receiving chronic VP
replacement and untreated LE rats exhibited cold-induced diuresis, with
peak increases in urine flow (V) of 63 +/- 12 (DIs) and 29 +/- 4 (LEs)
microliters.min-1 x 100 g body wt-1. LE rats acutely infused with VP
exhibited a diuresis at the two lower doses (peak V was 18 +/- 3 at the 30
and 18 +/- 4 microliters.min-1 x 100 g body wt-1 at the 60 pg.kg-1.min-1
dose), but the diuretic response was completely blunted at the uppermost
dose of VP. Cold-induced diuresis was absent at the lowest VP dose in the
acutely infused DI rats. A pressor response (30-36 mmHg) to CE was noted
with all treatment groups, including those that did not exhibit a diuresis.
No changes in glomerular filtration rate (GFR) with CE were observed. These
data suggest that when plasma VP levels are controlled by prolonged
infusion of VP in the DI rats, other mechanisms can operate to initiate
cold-induced diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
