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Purinoceptor-mediated calcium signaling in preglomerular smooth muscle cells. Hypertension 1999 Jan;33(1 Pt 2):195-200

Date

02/04/1999

Pubmed ID

9931104

DOI

10.1161/01.hyp.33.1.195

Scopus ID

2-s2.0-0032898185 (requires institutional sign-in at Scopus site)   44 Citations

Abstract

-The current studies were performed to determine the contribution of calcium mobilization and voltage-dependent calcium influx to the increase in [Ca2+]i elicited by ATP and UTP. Suspensions of freshly isolated smooth muscle cells were prepared from preglomerular microvessels by enzymatic digestion and loaded with the Ca2+-sensitive dye fura 2. The effect of ATP and UTP on [Ca2+]i was studied on single cells with standard microscope-based fluorescence photometry techniques. Resting [Ca2+]i averaged 80+/-3 nmol/L (n=219 single cells from 58 dispersions). ATP (100 micromol/L) increased [Ca2+]i to a peak value of 845+/-55 nmol/L (n=70 single cells from 38 dispersions) before stabilizing at 124+/-81 nmol/L. Similarly, 100 micromol/L UTP (n=39 single cells from 26 dispersions) stimulated a peak increase in [Ca2+]i of 1426+/-584 nmol/L before reaching a stable plateau of 123+/-10 nmol/L. The [Ca2+]i response to ATP and UTP was also assessed in the absence of extracellular calcium. In these studies, exposure to 100 micromol/L ATP induced a transient peak increase in [Ca2+]i, with the plateau phase being totally abolished. In contrast, exposure to 100 micromol/L UTP under calcium-free conditions resulted in no detectable change in the UTP-mediated increase in [Ca2+]i. The role of L-type calcium channels in the response was assessed with the calcium channel antagonist diltiazem. Incubation with diltiazem (10 micromol/L) markedly reduced the response to ATP, whereas the response to UTP was only slightly reduced. These data demonstrate that both ATP and UTP directly stimulate a biphasic increase in [Ca2+]i in renal microvascular smooth muscle cells. Furthermore, the data suggest that the elevation of [Ca2+]i elicited by ATP is largely dependent on calcium influx through L-type calcium channels, whereas the response to UTP appears to derive primarily from mobilization of calcium from intracellular stores.

Author List

Inscho EW, LeBlanc EA, Pham BT, White SM, Imig JD



MESH terms used to index this publication - Major topics in bold

Adenosine Triphosphate
Animals
Calcium
Cells, Cultured
Kidney Cortex
Kinetics
Male
Microcirculation
Muscle, Smooth, Vascular
Rats
Rats, Sprague-Dawley
Receptors, Purinergic
Signal Transduction
Uridine Triphosphate