NDLI: UTP activates small-conductance $Ca^{2+}-activated$ $K^{+}$ channels in murine detrusor $PDGFRα^{+}$ cells

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lee, Haeyeong Koh, Byoung H. Yamasaki, Evan George, Nikita E. Sanders, Kenton M. Koh, Sang Don
Description	Author Affiliation: Lee H ( Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.); Koh BH ( Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.); Yamasaki E ( Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.); George NE ( Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.); Sanders KM ( Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada.); Koh SD ( Department of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada skoh@medicine.nevada.edu.)
Abstract	Purines induce transient contraction and prolonged relaxation of detrusor muscles. Transient contraction is likely due to activation of inward currents in smooth muscle cells, and prolonged relaxation may be due to activation of small-conductance Ca(2+)-activated K(+) (SK) channels via P2Y1 receptors expressed by detrusor PDGF receptor (PDGFR) (+) cells. We investigated whether other subtypes of P2Y receptors are involved in the activation of SK channels in PDGFR (+) cells of detrusor muscles. Quantitative analysis of transcripts revealed that P2ry2, P2ry4, and P2ry14 are expressed in PDGFR (+) cells of P2ry1-deficient/enhanced green fluorescent protein (P2ry1(-/-)/eGFP) mice at similar levels as in wild-type mice. UTP, a P2Y2/P2Y4 agonist, activated large outward currents in detrusor PDGFR (+) cells. SK channel blockers and an inhibitor of phospholipase C completely abolished currents activated by UTP. In contrast, UTP activated nonselective cation currents in smooth muscle cells. Under current-clamp (current = 0), UTP induced significant hyperpolarization of PDGFR (+) cells. MRS2500, a selective P2Y1 antagonist, did not affect UTP-activated outward currents in PDGFR (+) cells from wild-type mice, and activation of outward currents by UTP was retained in P2ry1(-/-)/eGFP mice. As a negative control, we tested the effect of MRS2693, a selective P2Y6 agonist. This compound did not activate outward currents in PDGFR (+) cells, and currents activated by UTP were unaffected by MRS2578, a selective P2Y6 antagonist. The nonselective P2Y receptor blocker suramin inhibited UTP-activated outward currents in PDGFR (+) cells. Our data demonstrate that P2Y2 and/or P2Y4 receptors function, in addition to P2Y1 receptors, in activating SK currents in PDGFR (+) cells and possibly in mediating purinergic relaxation responses in detrusor muscles.
File Format	HTM / HTML
ISSN	1931857X
e-ISSN	15221466
DOI	10.1152/ajprenal.00156.2015
Journal	AJP: Renal Physiology
Issue Number	6
Volume Number	309
Language	English
Publisher	American Physiological Society
Publisher Date	2015-09-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Receptors, Purinergic P2 Signal Transduction Small-conductance Calcium-activated Potassium Channels Discipline Nephrology Receptors, Purinergic P2y1 Uridine Triphosphate Pharmacology Receptors, Purinergic P2y2 Adenosine Triphosphate Metabolism Drug Effects Muscle, Smooth Discipline Physiology Animals Myocytes, Smooth Muscle Receptor, Platelet-derived Growth Factor Alpha Patch-clamp Techniques Agonists Mice Urinary Bladder
Content Type	Text
Resource Type	Article
Subject	Physiology Urology

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