Nitric oxide inhibits Ca2+mobilization through cADP-ribose signaling in coronary arterial smooth muscle cells

American Journal of Physiology - Heart and Circulatory Physiology - Tập 279 Số 3 - Trang H873-H881 - 2000
Jiang-Zhou Yu1, David X. Zhang1, Ai-Ping Zou1, William B. Campbell1, Pin‐Lan Li1
1Departments of Pharmacology and Toxicology and Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226

Tóm tắt

The present study was designed to determine whether the cADP-ribose-mediated Ca2+signaling is involved in the inhibitory effect of nitric oxide (NO) on intracellular Ca2+mobilization. With the use of fluorescent microscopic spectrometry, cADP-ribose-induced Ca2+release from sarcoplasmic reticulum (SR) of bovine coronary arterial smooth muscle cells (CASMCs) was determined. In the α-toxin-permeabilized primary cultures of CASMCs, cADP-ribose (5 μM) produced a rapid Ca2+release, which was completely blocked by pretreatment of cells with the cADP-ribose antagonist 8-bromo-cADP-ribose (8-Br-cADPR). In intact fura 2-loaded CASMCs, 80 mM KCl was added to depolarize the cells and increase intracellular Ca2+concentration ([Ca2+]i). Sodium nitroprusside (SNP), an NO donor, produced a concentration-dependent inhibition of the KCl-induced increase in [Ca2+]i, but it had no effect on the U-46619-induced increase in [Ca2+]i. In the presence of 8-Br-cADPR (100 μM) and ryanodine (10 μM), the inhibitory effect of SNP was markedly attenuated. HPLC analyses showed that CASMCs expressed the ADP-ribosyl cyclase activity, and SNP (1–100 μM) significantly reduced the ADP-ribosyl cyclase activity in a concentration-dependent manner. The effect of SNP was completely blocked by addition of 10 μM oxygenated hemoglobin. We conclude that ADP-ribosyl cyclase is present in CASMCs, and NO may decrease [Ca2+]iby inhibition of cADP-ribose-induced Ca2+mobilization.

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American Journal of Physiology - Heart and Circulatory Physiology

Tập 279 Số 3

H873-H881

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