Reset of the osmotic threshold for vasopressin in rats fed a low NaCl, K-free diet

Activation of the renin-angiotensin system induced by feeding a low NaCl, K-free (LS) diet is associated with polydipsia and a chronic reduction in effective plasma osmolality (efPosm). We have recently shown that converting enzyme inhibition with enalapril (EP) abolishes polydipsia. The present study was designed to test the hypothesis that the osmotic threshold for vasopressin is reset in rats fed the LS diet and to examine the effect of EP on ambient and osmotically stimulated plasma vasopressin levels (PAvp). Animals were fed the LS diet or a control salt diet and treated with vehicle or the lowest dose of EP sufficient to prevent polydipsia (7.5 mg∙kg−1∙day−1) in rats fed the LS diet. PAVP and efPosm were measured under ambient conditions and after osmotic loading. Urine osmolality (Uosm) was measured under ambient conditions and after water loading. The chronic reduction in efPosm in LS rats was associated with the excretion of a Uosm 1–2 times greater than the corresponding Posm, PAVP similar to controls (LS, 2.27 ± 1.08 vs. control, 1.19 ± 0.22 pg/mL) and the ability to excrete a water load. Following osmotic loading, efPosm and PAVP increased significantly and similarly in both LS and control rats. EP administration had no effect on water intake, ambient efPosm and PAVP, and the AVP response to osmotic loading in rats fed the control diet. EP prevented polydipsia in LS rats, however it had no significant effect on ambient or osmotically stimulated PAVP or efPosm. These results provide evidence that the osmotic threshold for AVP is reset in rats fed the LS diet and although converting enzyme inhibition has a profound effect on water intake, angiotensin II does not appear to be the only variable affecting the osmotic threshold for AVP release.Key words: arginine vasopressin, antidiuretic hormone, osmotic threshold, plasma osmolality, rats, converting enzyme inhibition, angiotensin II, thirst.