Published online before print November 14, 2002, doi: 10.1161/01.RES.0000047507.22487.85
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Submitted on July 12, 2002
Revised on October 29, 2002
Accepted on November 4, 2002
Nicotinic Acid Adenine Dinucleotide Phosphate Mediates Ca2+ Signals and Contraction in Arterial Smooth Muscle via a Two-Pool Mechanism
François-Xavier Boittin ;
From the Department of Biomedical Sciences (F.-X.B., A.M.A.), School of Biology, University of St Andrews, Fife, and University Department of Pharmacology (A.G.), University of Oxford, UK.
* To whom correspondence should be addressed. E-mail: ame3{at}st-and.ac.uk.
Previous studies of arterial smooth muscle have shown that inositol 1,4,5-trisphosphate (IP3) and cyclic ADP-ribose mobilize Ca2+ from the sarcoplasmic reticulum. In contrast, little is known about Ca2+ mobilization by nicotinic acid adenine dinucleotide phosphate, a pyridine nucleotide derived from 
-NADP+. We show here that intracellular dialysis of nicotinic acid adenine dinucleotide phosphate (NAADP) induces spatially restricted "bursts" of Ca2+ release that initiate a global Ca2+ wave and contraction in pulmonary artery smooth muscle cells. Depletion of sarcoplasmic reticulum Ca2+ stores with thapsigargin and inhibition of ryanodine receptors with ryanodine, respectively, block the global Ca2+ waves by NAADP. Under these conditions, however, localized Ca2+ bursts are still observed. In contrast, xestospongin C, an IP3 receptor antagonist, had no effect on Ca2+ signals by NAADP. We propose that NAADP mobilizes Ca2+ via a 2-pool mechanism, and that initial Ca2+ bursts are amplified by subsequent sarcoplasmic reticulum Ca2+ release via ryanodine receptors but not by IP3 receptors.
Key words: NAADP • calcium • smooth muscle • sarcoplasmic reticulum • ryanodine receptors
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