Abstract
The current study examined the role of extracellular Ca 2+, calmodulin and myosin light-chain kinase (MLCK) in pervanadate-induced constriction of cannulated, pressurized rat cremaster arterioles. Pervanadate (0.03–100 μM) induced a concentration-dependent constriction of arterioles that was significantly attenuated ( P<0.05) by the tyrosine kinase inhibitor tyrphostin 47 (30 μM). The L-type voltage-sensitive Ca 2+ channel antagonists verapamil (10 μM) and nifedipine (1 μM) dilated vessels possessing myogenic tone but had no demonstrable effect on pervanadate constriction, while a higher concentration of nifedipine (10 μM) reduced constriction by approximately 50%. Pervanadate-induced contractions were reduced by the calmodulin inhibitor W-7 ( N-(6-aminohexyl)-chloro-1-naphtalene sulphonamide, 50 μM) and the MLCK inhibitor ML-7 (1-(5-iodonaphthalene-1-sulfonyl)-1 H-hexahydro-1,4-diazepine, 10 or 30 μM). Removal of extracellular Ca 2+ abolished the contractile effect of pervanadate. Measurement of changes in arteriolar wall [Ca 2+] using the Ca 2+ sensitive dye Fura-2 showed that pervanadate did not increase [Ca 2+] during arteriolar constriction. These observations suggest that pervanadate-induced contraction of smooth muscle in the cremaster arteriole involves Ca 2+/calmodulin-dependent myosin phosphorylation and possibly sensitization of the contractile apparatus to Ca 2+.
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