Potassium Channels in the Renal Circulation

Stockand, James D.; Sansom, Steven C.

doi:10.1007/978-1-4615-1303-2_28

Cited by 1 publication

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“…All smooth muscle cells, including those of the renal vessels [11-13], contain BK. Because of inaccessibility to patch clamping, BK have been difficult to identify and study in vivo or in isolated glomerular cells.…”

Section: Localization Of Bk In the Kidneymentioning

confidence: 99%

Interacting influence of diuretics and diet on BK channel-regulated K homeostasis

Wen

Cornelius

Sansom

2014

Current Opinion in Pharmacology

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Large conductance, Ca-activated K channels are abundantly located in cells of vasculature, glomerulus and distal nephron, where they are involved in maintaining blood volume, blood pressure and K homeostasis. In mesangial cells and smooth muscle cells of vessels, the BK-α pore associates with BK-β1 subunits and regulates contraction in a Ca-mediated feedback manner. The BK-β1 also resides in connecting tubule cells of the nephron. BK-β1 knockout mice (β1KO) exhibit fluid retention, hypertension, and compromised K handling. The BK-α/β4resides in acid/base transporting intercalated cells (IC) of the distal nephron, where they mediate K secretion in mammals on a high K, alkaline diet. BK-α expression in IC is increased by a high K diet via aldosterone. The BK-β4 subunit and alkaline urine are necessary for the luminal expression and function of BK-α in mouse IC. In distal nephron cells, membrane BK-α expression is inhibited by WNK4 in in vitro expression systems, indicating a role in the hyperkalemic phenotype in patients with familial hyperkalemic hypertension type 2 (FHHt2). β1KO and BK-β4 knockout mice (β4KO) are hypertensive because of exaggerated ENaC-mediated Na retention in an effort to secrete K via only ROMK. BK hypertension is resistant to thiazides and furosemide, and would be more amenable to ENaC and aldosterone inhibiting drugs. Activators of BK-α/β1 or BK-α/β4 might be effective blood pressure lowering agents for a subset of hypertensive patients. Inhibitors of renal BK would effectively spare K in patients with Bartter Syndrome, a renal K wasting disease.

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Section: Localization Of Bk In the Kidneymentioning

confidence: 99%