NDLI: KATP channels are not essential for pressure-dependent control of renin secretion

Content Provider	Springer Nature Link
Author	Jensen, Boye L. Gambaryan, Stepan Scholz, Holger Kurtz, Armin
Copyright Year	1998
Abstract	This study aimed to investigate the functional role of ATP-sensitive K+ (KATP) channels in the control of renin secretion by renal perfusion pressure. We studied the effect of openers and blockers of KATP-channels on basal- and low-pressure-induced renin secretion from isolated perfused rat kidneys (IPRK). Cromakalim (0.1–10 μM) stimulated basal renin secretion up to threefold and caused vasorelaxation in the IPRK. Both effects of cromakalim were attenuated by glibenclamide. Cromakalim stimulated renin secretion from isolated juxtaglomerular (JG) cells and from microdissected afferent arterioles, all of which suggests that K ATP channel openers stimulate renin secretion at the level of JG cells. A decrease in the perfusion pressure from 13.3 to 9.33 kPa (100 mmHg to 70 mmHg) increased renin secretion twofold, and cromakalim further increased renin secretion. At 5.33 kPa (40 mmHg) renin secretion was increased sevenfold and was not further enhanced by cromakalim. The low-pressure-induced stimulation of renin secretion was not changed by glibenclamide. Finally, the dependence on calcium of the cromakalim-induced stimulation of renin was examined. Addition of the calcium antagonist amlodipine to the perfusate stimulated renin secretion, and in this situation cromakalim had no further effect. The stimulation of renin secretion by cromakalim in the IPRK was markedly attenuated by angiotensin II (1 nM). These results suggest that cromakalim could stimulate renin secretion through a pathway that includes a decrease in JG cell calcium. KATP channels are not essentially involved in pressure-sensitive renin secretion.
Starting Page	670
Ending Page	677
Page Count	8
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	435
Issue Number	5
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	1998-03-02
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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