Stimulation of renin secretion by potassium-channel activation with cromakalim

Ferrier, Claudia; Kurtz, Armin; Lehner, Paul J.; Shaw, Sidney; Pusterla, C; Saxenhofer, Hermann; Weidmann, P

doi:10.1007/bf00558067

Cited by 33 publications

(28 citation statements)

References 22 publications

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“…A possible mediator could be endothelium-derived hyperpolarizing factor which is produced by EC in response to ATP (31) and which is thought to open (ATP-sensitive) potassium channels in VSMC (32). This idea would fit with the observation that the potassium channel opener cromakalim exerts a stimulatory effect on renin secretion from isolated rat JG cells (33).…”

Section: Discussionmentioning

confidence: 64%

Endothelial cells modulate renin secretion from isolated mouse juxtaglomerular cells.

Kurtz

Kaissling²,

Busse³

et al. 1991

J. Clin. Invest.

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Utilizing cocultures of mouse renal juxtaglomerular cells with bovine microvascular endothelial cells, we have examined whether endothelial cells exert direct influence on renin secretion from renal juxtaglomerular cells.In the presence of endothelial cells both spontaneous and forskolin (10 isM) or isoproterenol (10 sM) stimulated renin release were markedly attenuated. The stimulatory effect ofthe calmodulin antagonist calmidazolium (10 pM) on renin secretion was not altered by endothelial cells, whereas the stimulatory effect of ethylisopropylamiloride (50 pM) an inhibitor of sodium-proton exchange was enhanced in the presence of endothelial cells. Indomethacin (10 1M) and NG-monomethyl-l-arginine (NMMA) (1 mM) used to inhibit cyclooxygenase activity and production of endothelium-derived relaxing factor (EDRF) decreased spontaneous renin release in the presence of endothelial cells only, but had no effect on forskolin stimulated

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Section: Discussionmentioning

confidence: 64%

Endothelial cells modulate renin secretion from isolated mouse juxtaglomerular cells.

Kurtz

Kaissling²,

Busse³

et al. 1991

J. Clin. Invest.

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“…In addition, an increase in the extracellular K ϩ concentration or an inhibition of K ϩ channels not only depolarizes JG cells, but also suppresses renin release (158,269,480,487). On the other hand, the membrane hyperpolarization induced by K ϩ channel activation or Cl Ϫ channel inhibition is accompanied by a stimulated renin secretion (227,239,396,403,615). Furthermore, the pharmacological inhibition of the Na ϩ -K ϩ -2Cl Ϫ cotransport activity using furosemide leads to the hyperpolarization of single JG cells while concomitantly stimulating renin exocytosis (128).…”

Section: B Electrical Properties Of Juxtaglomerular Cellsmentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

232

277

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The protease renin is the key enzyme of the renin-angiotensin-aldosterone cascade, which is relevant under both physiological and pathophysiological settings. The kidney is the only organ capable of releasing enzymatically active renin. Although the characteristic juxtaglomerular position is the best known site of renin generation, renin-producing cells in the kidney can vary in number and localization. (Pro)renin gene transcription in these cells is controlled by a number of transcription factors, among which CREB is the best characterized. Pro-renin is stored in vesicles, activated to renin, and then released upon demand. The release of renin is under the control of the cAMP (stimulatory) and Ca2+(inhibitory) signaling pathways. Meanwhile, a great number of intrarenally generated or systemically acting factors have been identified that control the renin secretion directly at the level of renin-producing cells, by activating either of the signaling pathways mentioned above. The broad spectrum of biological actions of (pro)renin is mediated by receptors for (pro)renin, angiotensin II and angiotensin-( 1 – 7 ).

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“…These channels are activated by an increase in the cyclic AMP concentration (23). Third, renin-producing cells appear to have KATP channels, the activation of which causes hyperpolarization of the cells (18,35,71). In addition, renin-producing cells likely possess a high number of calcium-activated chloride channels (45) as well as Ltype calcium channels (23).…”

Section: Electrical Characteristics Of Reninsecreting Juxtaglomerularmentioning

confidence: 99%

Renin Release

et al. 2007

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The aspartyl-protease renin is the key regulator of the renin-angiotensin-aldosterone system, which is critically involved in salt, volume, and blood pressure homeostasis of the body. Renin is mainly produced and released into circulation by the so-called juxtaglomerular epithelioid cells, located in the walls of renal afferent arterioles at the entrance of the glomerular capillary network. It has been known for a long time that renin synthesis and secretion are stimulated by the sympathetic nerves and the prostaglandins and are inhibited in negative feedback loops by angiotensin II, high blood pressure, salt, and volume overload. In contrast, the events controlling the function of renin-secreting cells at the organ and cellular level are markedly less clear and remain mysterious in certain aspects. The unravelling of these mysteries has led to new and interesting insights into the process of renin release.

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Stimulation of renin secretion by potassium-channel activation with cromakalim

Cited by 33 publications

References 22 publications

Endothelial cells modulate renin secretion from isolated mouse juxtaglomerular cells.

Endothelial cells modulate renin secretion from isolated mouse juxtaglomerular cells.

Physiology of Kidney Renin

Renin Release

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