Regulation of luminal alkalinization and acidification in the cortical collecting duct by angiotensin II

• Published in: American journal of physiology. Renal physiology Vol. 269; no. 5 Pt 2; pp. F730 - F738
• Main Authors: Weiner, I D, New, A R, Milton, A E, Tisher, C C
• Format: Journal Article
• Language: English
• Published: United States 01.11.1995
• Subjects: Acids - metabolism; Alkalies - metabolism; Angiotensin I - metabolism; Angiotensin II - pharmacology; Angiotensin Receptor Antagonists; Animals; Bicarbonates - metabolism; Biphenyl Compounds - pharmacology; Female; Hydrogen-Ion Concentration; Imidazoles - pharmacology; In Vitro Techniques; Kidney Tubules, Collecting - drug effects; Kidney Tubules, Collecting - metabolism; Losartan; Osmolar Concentration; Perfusion; Rabbits; Tetrazoles - pharmacology
• ISSN: 0002-9513; 1931-857X; 1522-1466
• DOI: 10.1152/ajprenal.1995.269.5.f730

Angiotensin II (ANG II) regulates whole kidney ion transport, yet its effects in the collecting duct are unknown. The purpose of these studies was to determine whether ANG II regulates luminal alkalinization and acidification in the rabbit cortical collecting duct (CCD). The rate of luminal alkalinization or acidification was measured as the rate of change of luminal fluid pH under stop-flow conditions using in vitro microperfused CCD segments. Outer CCD alkalinized the luminal fluid, consistent with net HCO3- secretion. Addition of ANG II, 10(-7) M, to the peritubular solution for 30 min significantly stimulated luminal alkalinization. The stimulatory effect of ANG II was not due to time-dependent effects and was blocked by peritubular addition of the ANG II type 1 (AT1) receptor antagonist, losartan, at 10(-6) M. Losartan, 10(-6) M, when added to the peritubular solution, did not alter the rate of luminal alkalinization independent of ANG II. In contrast, peritubular ANG II, 10(-7) M, did not alter inner CCD luminal acidification. Addition of ANG II to the peritubular solution at the lower concentration of 10(-10) M did not alter the rates of luminal alkalinization and acidification in the outer and inner CCD, respectively. Peritubular ANG II, 10(-7) M, but not vehicle, stimulated B cell apical HCO3- secretion occurring in response to peritubular Cl- removal. These studies demonstrate that ANG II acts through a basolateral AT1 receptor to stimulate outer CCD luminal alkalinization via, at least in part, B cell stimulation.