EFFECTS OF VASODILATOR DRUGS, ALKALINE PHOSPHTASE, AND CYCLIC AMP‐DEPENDENT PROTEIN KINASE ON THE 45CALCIUM UPTAKE OF SARCOLEMMAL MICROSOMES FROM HUMAN UMBILICAL ARTERIES

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Abstract
1 A microsomal fraction was prepared from human umbilical arteries by differential centrifugation. The preparation was capable of an oxalate-stimulated Ca2+ uptake at a mean rate of 0.74 nmol Ca2+ mg−1 protein min−1 which could be inhibited by a Ca2+ ionophore, A 23 187, and by Tween 80. 2 The rate of Ca2+ uptake in the fractions obtained by density gradient fractionation paralleled 5′-nucleotidase activity suggesting that vesicles of predominantly sarcolemmal origin were responsible for the microsomal Ca2+ uptake. 3 Cyclic adenosine 3′,5′-monophosphate-dependent protein kinase enhanced membrane phosphorylation but did not affect Ca2+ uptake. Preincubation with alkaline phosphatase reduced membrane phosphorylation to a greater extent than Ca2+ uptake. These data are not in favour of a close correlation between Ca2+ uptake and phosphorylation. 4 None of 15 vasodilator drugs (bencyclane, carbocromen, diazoxide, dilazep, hydralazine, indapamide, isosorbide dinitrate, methyl-isobutyl-xanthine, minoxidil, naftidrofuryl, nitroglycerine, prenylamine, sodium nitroprusside, tetracaine, and verapamil) had any effect on Ca2+ uptake at 10−5 m. This suggests that vasodilator drugs do not act by a direct influence on the Ca2+ pumps of vascular smooth muscle cells.