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Circulation Research. 2002
Published online before print August 29, 2002, doi: 10.1161/01.RES.0000035060.98415.4B
A more recent version of this article appeared on September 20, 2002
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Submitted on July 17, 2002
Revised on August 14, 2002
Accepted on August 15, 2002

Evoked and Spontaneous Purinergic Junctional Ca2+ Transients in Rat Small Arteries

Christine Lamont and W. Gil Wier *

From the Department of Physiology, School of Medicine, University of Maryland, Baltimore, Md.

* To whom correspondence should be addressed. E-mail: gwier001{at}umaryland.edu.

Confocal microscopy of fluo-4 fluorescence in pressurized rat mesenteric small arteries subjected to low-frequency electrical field stimulation revealed Ca2+ transients in perivascular nerves and novel, spatially localized Ca2+ transients in adjacent smooth muscle cells. These muscle Ca2+ transients occur with a very brief latency to the stimulus pulse (most <3 ms). They are wider ({approx}5 µm) and last longer (t1/2, 145 ms) than Ca2+ sparks. They are abolished by the purinergic receptor (P2X) antagonist suramin, but they are totally unaffected by the {alpha}1-adrenoceptor antagonist prazosin or by capsaicin (which inhibits the function of perivascular sensory nerves). We conclude that these novel Ca2+ transients represent Ca2+ entering smooth muscle cells through P2X receptors activated by ATP released from sympathetic nerves, and we therefore call them "junctional Ca2+ transients" or jCaTs. As expected from spontaneous neurotransmitter release, jCaTs also occur spontaneously, with characteristics identical to evoked jCaTs. Visualization of sympathetic neurotransmission shows that purinergic components dominate at low frequencies of sympathetic nerve fiber activation.


Key words: calcium transient • smooth muscle • artery




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