Effects of Cromakalim on Renal Hemodynamics and Function in Dogs

Takahashi, Toshiaki; Hasui, Kouichi; Shoji, Tetsuo; Fukui, Kiyoshi; Itoh, Hiroshi; Abe, Youichi

doi:10.1097/00005344-199102000-00017

Cited by 6 publications

(6 citation statements)

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“…Amongst these specific potassium channels only the role of K ATP channels has been considered. Consistent evidence has been obtained from in vivo [11,30] and in vitro [3,14] experiments that activation of K ATP channels stimulates renin secretion. Notably, inhibiting K ATP channels with glibenclamide does not affect renin secretion under basal and under stimulated conditions [14], rendering the role of K ATP channels in the physiological control of renin secretion less clear.…”

Section: Introductionsupporting

confidence: 77%

Role of potassium channels in the control of renin secretion from isolated perfused rat kidneys

Kurtz

Hamann

Götz

2000

Pflugers Arch - Eur J Physiol

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This study aimed to assess the relevance of specific potassium channels, such as inwardly or outwardly rectifying and calcium-regulated potassium channels, to the control of renin secretion. For this purpose we examined the effects of the K+ channel blockers 4-aminopyridine (1 mmol/l), barium (100 micromol/l), tetraethylammonium (2 mmol/l) and apamin (200 nmol/l) on basal renin secretion, on renin secretion stimulated by isoproterenol (10 nmol/l) and on the inhibition of renin secretion by angiotensin II (100-300 pmol/l) in the isolated rat kidney perfused at constant pressure. Whilst all four K+ channel blockers increased renal vascular resistance, only 4-aminopyridine and barium attenuated isoproterenol-stimulated renin secretion in an additive fashion and augmented the inhibitory effect of angiotensin II. These effects of K+ channel blockers were not changed by the L-type calcium channel blocker amlodipine (5 pmol/l), indicating that their effects on renin secretion are not due to voltage-operated calcium influx. Our data, moreover, suggest that potassium efflux from renal juxtaglomerular cells is not important for the inhibitory action of angiotensin II on renin secretion. As a consequence it appears that the membrane potential of renal juxtaglomerular cells per se is relevant to renin secretion such that membrane depolarization inhibits the exocytosis of renin whilst hyperpolarization favors renin secretion. By their activity, potassium channels can contribute to membrane hyperpolarization and thus facilitate renin secretion.

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Section: Introductionsupporting

confidence: 77%

Role of potassium channels in the control of renin secretion from isolated perfused rat kidneys

Kurtz

Hamann

Götz

2000

Pflugers Arch - Eur J Physiol

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“…Maneuvers that lead to membrane hyperpolarization, such as potassium channel opening or moderate increases in the extracellular potassium concentration [because of the existence of inwardly rectifying potassium currents (K ir channels) (100)] in JG cells, are associated with an increase in renin release (113)(114)(115). Conversely, membranedepolarizing maneuvers such as larger increases in extracellular potassium (116,117), inhibition of K ir (100,117), or activation of chloride channels (100,118) are associated with reduced renin release (116).…”

Section: Membrane Potentialmentioning

confidence: 99%

Renin Release: Sites, Mechanisms, and Control

Kurtz

2011

Annu. Rev. Physiol.

102

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In the adult organism, systemically circulating renin almost exclusively originates from the juxtaglomerular cells in the afferent arterioles of the kidneys. These cells share similarities with pericytes and myofibro-blasts. They store renin in a vesicular network and granules and release it in a regulated fashion. The release mode of renin is not understood; in particular, the involvement of SNARE proteins is unknown. Renin release is acutely increased via the cAMP signaling pathway, which is triggered mainly by catecholamines and other G(s)-coupled agonists, and is inhibited by calcium-related pathways that are commonly activated by vasoconstrictors. Renin release from juxtaglomerular cells is directly modulated in an inverse fashion by the blood pressure inside the afferent arterioles and by the chloride content in the tubule fluid at the macula densa segment of the distal tubule. Renin release is stimulated by nitric oxide and by prostanoids released by neighboring endothelial and macula densa cells. Steady-state renin concentrations in the plasma are determined essentially by the number of renin-producing cells in the afferent arterioles, which changes in parallel with challenges to the renin-angiotensin-aldosterone system.

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“…Cromakalim and calcium channel blockers are suggested to act on the same pathway to cause vasodilation and natriuresis in the dog kidney (Tamaki et al 1991). Therefore cromakalim could mimic the inhibitory effect of nifedipine on the HS-induced responses.…”

Section: Introductionmentioning

confidence: 99%

“…A potassium channel opener, cromakalim, hyperpolarizes membrane potential (Weir & Weston 1986) which could interfere with the voltage-dependent calcium channels in vascular smooth muscle cells (Nakao et al 1988). Cromakalim and calcium channel blockers are suggested to act on the same pathway to cause vasodilation and natriuresis in the dog kidney (Tamaki et al 1991). Therefore cromakalim could mimic the inhibitory effect of nifedipine on the HS-induced responses.…”

Section: Introductionmentioning

confidence: 99%

Cromakalim Suppresses Hypertonic Saline‐induced Renal Vasoconstriction in Anaesthetized Dogs

Hirano

Hisa

Satoh

1995

Clin Exp Pharma Physio

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1. Intrarenal arterial infusion of hypertonic saline (HS) transiently increased and then gradually reduced renal blood flow (RBF) in anaesthetized dogs. Glomerular filtration rate (GFR) but not filtration fraction decreased at the end of the infusion. 2. In the presence of a potassium channel opener cromakalim (0.3 microgram/kg per min), HS infusion failed to reduce RBF; the initial increase in RBF was maintained throughout the infusion. Since cromakalim also prevented the decrease in GFR, HS infusion lowered filtration fraction. 3. The results suggest that cromakalim inhibits both pre-and postglomerular vasoconstriction induced by HS infusion.

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Effects of Cromakalim on Renal Hemodynamics and Function in Dogs

Cited by 6 publications

References 0 publications

Role of potassium channels in the control of renin secretion from isolated perfused rat kidneys

Role of potassium channels in the control of renin secretion from isolated perfused rat kidneys

Renin Release: Sites, Mechanisms, and Control

Cromakalim Suppresses Hypertonic Saline‐induced Renal Vasoconstriction in Anaesthetized Dogs

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