Role of chloride in constriction of descending vasa recta by angiotensin II
| Autor: | Malcolm R. Turner, Zhong Zhang, Kristie Rhinehart, James M. C. Huang, Thomas L. Pallone |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
medicine.medical_specialty
Physiology Membrane Potentials Potassium Chloride Constriction Rats Sprague-Dawley Chlorides Chloride Channels Physiology (medical) Internal medicine Renin–angiotensin system Renal medulla medicine Animals Patch clamp Membrane potential Kidney Medulla Chemistry Angiotensin II Niflumic acid Niflumic Acid Vasa recta Isoxazoles Glycolates Rats medicine.anatomical_structure Endocrinology Vasoconstriction Barbiturates Calibration cardiovascular system Blood Vessels medicine.drug |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 280:R1878-R1886 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.2001.280.6.r1878 |
| Popis: | We investigated the dependence of ANG II (10−8 M)-induced constriction of outer medullary descending vasa recta (OMDVR) on membrane potential (Ψm) 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 [DiBAC4(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 DiBAC4(3) in unstimulated vessels, neither changing extracellular Cl− concentration ([Cl−]) nor exposure to the chloride channel blocker indanyloxyacetic acid 94 (IAA-94; 30 μM) affected Ψm. In contrast, IAA-94 repolarized OMDVR pretreated with ANG II. Neither IAA-94 (30 μM) nor niflumic acid (30 μM, 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. |
| Databáze: | OpenAIRE |
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