Regulation of acid-base transporters by vasopressin in the kidney collecting duct of Brattleboro rat.
Regulation of acid-base transporters by vasopressin in the kidney collecting duct of Brattleboro rat.
复制标题
布拉特尔伯勒大鼠肾集合管中加压素对酸碱转运蛋白的调节。
DOI:
10.1159/000093305
复制
发表时间:
2006
影响因子:
4.2
通讯作者:
Soleimani,Manoocher
中科院分区:
文献类型:
--
作者:
Amlal,Hassane;Sheriff,Sulaiman;Faroqui,Somia;Ma,Liyun;Barone,Sharone;Petrovic,Snezana;Soleimani,Manoocher
AimThe objective of these studies was to examine the effects of long-term vasopressin treatment on acid-base transporters in the collecting duct of rat kidney.MethodsBrattleboro rats were placed in metabolic cages and treated with daily injections of 1-desamino-8-D-arginine vasopressin (dDAVP), a selective V 2-receptor agonist, or its vehicle (control) for up to 8 days.ResultsdDAVP treatment resulted in a significant reduction in serum bicarbonate concentration, and caused the upregulation of key ammoniagenesis enzymes, along with increased urinary NH 4+ excretion. Northern hybridization and immunofluorescence labeling indicated a significant increase (+ 80%) in mRNA expression of the apical Cl–/HCO 3–exchanger pendrin (PDS), along with a sharp increase in its protein abundance in B-type intercalated cells in the cortical collecting duct in dDAVP-treated rats. In the inner medullary collecting duct, the abundance of basolateral Cl–/HCO 3–exchanger (AE1) and apical H+-ATPase was significantly reduced in dDAVP-treated rats. Kidney renin mRNA increased significantly and correlated with an increase in serum aldosterone levels in dDAVP-injected rats. Serum corticosterone levels were, however, reduced and correlated with increased mRNA levels of renal 11β-hydroxysteroid dehydrogenase-2 (11β-HSD2) and decreased mRNA expression of 11β-hydroxylase in the adrenal gland of dDAVP-injected rats.ConclusionChronic administration of dDAVP to Brattleboro rats is associated with the upregulation of PDS and downregulation of H+-ATPase and AE1 in the collecting duct, along with increased ammoniagenesis. Stimulation of the renin-angiotensin-aldosterone system and/or decreased glucocorticoid levels likely plays a role in the transduction of these effects.