MECHANISMS FOR THE DIURESIS OF ACUTE COLD-EXPOSURE - ROLE FOR VASOPRESSIN

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) mul . min- 1 . 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 mul . min-1 . 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. These do not include an elevated GFR, nor is the diuresis of acute CE a pressure diuresis. The finding of low doses of VP that would blunt the appearance of a diuretic response may reveal more about the ability of an antidiuretic agent to oppose a diuresis (regardless of its origin) than it does about the physiology of cold-induced diuresis.