Abstract
The addition of 1 X 10(-3) M or 1 X 10(-2) M 2-mercaptoethanol (2-MEt), a sulfhydryl reagent, produced a leftward displacement (potentiation) of the dose-response curves of mesenteric arterial strips for histamine, norepinephrine, serotonin, angiotensin II, prostaglandin F2 alpha and KCl. N-ethylmaleimide abolished the 2-MEt-induced potentiation of the arterial responses. Dithiothreitol (DTT) and cysteine also potentiated the contraction by these agonists in mesenteric arterial strips, suggesting that the sulfhydryl group plays a role in the arterial responses to various contractile agonists. In contrast to the mesenteric arterial strips, 2-MEt abolished the contraction by angiotensin II without greatly affecting contraction by norepinephrine in the thoracic aorta, femoral, renal and carotid arterial strips. These data suggest that there are regional differences in the responsiveness of rabbit arteries to sulfhydryl reagents. In mesenteric arterial strips treated with 1 X 10(-6) M histamine, 6 X 10(-8) M norepinephrine or 1 X 10(-9) M angiotensin II after exposure to Ca2+-free Krebs' bicarbonate solutions containing 0.1 mM EGTA, the addition of 2.5 mM CaCl2 caused a contraction (agonist-induced Ca2+-contraction). Sulfhydryl reagents potentiated each agonist-induced Ca2+-contraction in this artery. Moreover, in thoracic aortic strips, sulfhydryl reagents enhanced only histamine-induced Ca2+-contraction and attenuated norepinephrine- and angiotensin II-induced Ca2+-contractions. It is concluded that the reduction of a disulfide bond of the arterial strips to a sulfhydryl group affects the pharmacological receptor activities of the strips and that the changes in the receptor activities may be related to the changes in the transmembrane influx of calcium.
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