Constriction of outer medullary descending vasa recta by angiotensin II involves pericyte depolarization mediated partly by increased chloride channel activity.
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 bis1,3-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.
Zhang et al. (2001) studied this question.