title: Role of chloride in constriction of descending vasa recta by angiotensin II.
abstract: We investigated the dependence of ANG II (10(-8) M)-induced constriction of outer medullary descending vasa recta (OMDVR) on membrane potential (Psim) and chloride ion. ANG II depolarized OMDVR, as measured by fully loading them with the voltage-sensitive dye bis[1,3-dibutylbarbituric acid-(5)] trimethineoxonol [DiBAC(4)(3)] or selectively loading their pericytes. ANG II was also observed to depolarize pericytes from a resting value of -55.6 +/- 2.6 to -26.2 +/- 5.4 mV when measured with gramicidin D-perforated patches. When measured with DiBAC(4)(3) in unstimulated vessels, neither changing extracellular Cl(-) concentration ([Cl(-)]) nor exposure to the chloride channel blocker indanyloxyacetic acid 94 (IAA-94; 30 microM) affected Psim. In contrast, IAA-94 repolarized OMDVR pretreated with ANG II. Neither IAA-94 (30 microM) nor niflumic acid (30 microM, 1 mM) affected the vasoactivity of unstimulated OMDVR, whereas both dilated ANG II-preconstricted vessels. Reduction of extracellular [Cl(-)] from 150 to 30 meq/l enhanced ANG II-induced constriction. Finally, we identified a Cl(-) channel in OMDVR pericytes that is activated by ANG II or by excision into extracellular buffer. We conclude that constriction of OMDVR by ANG II involves pericyte depolarization due, in part, to increased activity of chloride channels.
authors.affiliation: Division of Nephrology, University of Maryland School of Medicine, Baltimore, Maryland 21201-1595, USA.
authors.forename: Z
authors.initials: Z
authors.lastname: Zhang
authors.forename: J M
authors.initials: JM
authors.lastname: Huang
authors.forename: M R
authors.initials: MR
authors.lastname: Turner
authors.forename: K L
authors.initials: KL
authors.lastname: Rhinehart
authors.forename: T L
authors.initials: TL
authors.lastname: Pallone
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D001463:Barbiturates; D001808:Blood Vessels / Q000187:drug effects / Q000502:physiology; D002138:Calibration; D018118:Chloride Channels / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology / Q000502:physiology*; D006016:Glycolates / Q000494:pharmacology; D007555:Isoxazoles; D007679:Kidney Medulla / Q000098:blood supply*; D008564:Membrane Potentials / Q000187:drug effects; D009544:Niflumic Acid / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects
chemical_list: D001463:Barbiturates; D018118:Chloride Channels; D002712:Chlorides; D006016:Glycolates; D007555:Isoxazoles; C052795:bis(1,3-dibutylbarbiturate)trimethine oxonol; D000804:Angiotensin II; D009544:Niflumic Acid; C015765:MK 473; D011189:Potassium Chloride