deamino-arginine-vasopressin and Potassium-Deficiency

The association between diabetes insipidus (DI) and chronic dietary K

Topics: Animals; Antidiuretic Agents; Aquaporin 2; Deamino Arginine Vasopressin; Diabetes Insipidus, Nephrogenic; Disease Models, Animal; Drug Resistance; Female; Kidney; Male; Mice, Inbred C57BL; Phosphorylation; Potassium Deficiency; Potassium, Dietary; Risk Factors; Sex Characteristics; Water-Electrolyte Balance

The purpose of the present studies was to determine the effects of high-dose aldosterone and dDAVP treatment on renal aquaporin-2 (AQP2) regulation and urinary concentration. Rats were treated for 6 days with either vehicle (CON; n = 8), dDAVP (0.5 ng/h, dDAVP, n = 10), aldosterone (Aldo, 150 microg/day, n = 10) or combined dDAVP and aldosterone treatment (dDAVP+Aldo, n = 10) and had free access to water with a fixed food intake. Aldosterone treatment induced hypokalemia, decreased urine osmolality, and increased the urine volume and water intake in ALDO compared with CON and dDAVP+Aldo compared with dDAVP. Immunohistochemistry and semiquantitative laser confocal microscopy revealed a distinct increase in basolateral domain AQP2 labeling in cortical collecting duct (CCD) principal cells and a reduction in apical domain labeling in Aldo compared with CON rats. Given the presence of hypokalemia in aldosterone-treated rats, we studied dietary-induced hypokalemia in rats, which also reduced apical AQP2 expression in the CCD but did not induce any increase in basolateral AQP2 expression in the CCD as observed with aldosterone treatment. The aldosterone-induced basolateral AQP2 expression in the CCD was thus independent of hypokalemia but was dependent on the presence of sodium and aldosterone. This redistribution was clearly blocked by mineralocorticoid receptor blockade. The increased basolateral expression of AQP2 induced by aldosterone may play a significant role in water metabolism in conditions with increased sodium reabsorption in the CCD.

Topics: Aldosterone; Angiotensin II; Animals; Aquaporin 2; Deamino Arginine Vasopressin; Drinking; Eating; Homeostasis; Hypokalemia; Immunoblotting; Immunohistochemistry; Kidney Cortex; Kidney Tubules, Collecting; Male; Microscopy, Immunoelectron; Phosphorylation; Potassium Deficiency; Rats; Rats, Sprague-Dawley; Rats, Wistar; Renal Agents; Serine; Subcellular Fractions; Water

Rat collecting ducts exhibit type I or type III K(+)-ATPase activities when animals are fed a normal (NK) or a K(+)-depleted diet (LK). This study aimed at determining functionally the cell origin of these two K(+)-ATPases. For this purpose, we searched for an effect on K(+)-ATPases of hormones that trigger cAMP production in a cell-specific fashion. The effects of 1-deamino-8-D-arginine vasopressin (dD-AVP), calcitonin, and isoproterenol in principal cells, alpha-intercalated cells, and beta-intercalated cells of cortical collecting duct (CCD), respectively, and of dD-AVP and glucagon in principal and alpha-intercalated cells of outer medullary collecting duct (OMCD), respectively, were examined. In CCDs, K(+)-ATPase was stimulated by calcitonin and isoproterenol in NK rats (type I K(+)-ATPase) and by dD-AVP in LK rats (type III K(+)-ATPase). In OMCDs, dD-AVP and glucagon stimulated type III but not type I K(+)-ATPase. These hormone effects were mimicked by the cAMP-permeant analog dibutyryl-cAMP. In conclusion, in NK rats, cAMP stimulates type I K(+)-ATPase activity in alpha- and beta-intercalated CCD cells, whereas in LK rats it stimulates type III K(+)-ATPase in principal cells of both CCD and OMCD and in OMCD intercalated cells.

Topics: Adenosine Triphosphatases; Animals; Cation Transport Proteins; Deamino Arginine Vasopressin; Enzyme Inhibitors; Glucagon; Hormones; Imidazoles; Kidney Tubules, Collecting; Male; Potassium Deficiency; Rats; Rats, Sprague-Dawley; Rubidium