Endothelium-Derived Relaxing Factor
نویسنده
چکیده
The vascular effects of endothelin-1 (ET) in humans were investigated by brachial artery infusions of ET into 25 healthy volunteers. Forearm blood flow increased from a mean±SD value of 2.3± 1.5 to 2.5± 1.5 ml/min/100 ml forearm tissue (n=25, p<0.05) in response to low dose (0.5 ng/min/100 ml forearm tissue) ET infusion and decreased to 1.78±1.3 and 1.1±0.9 ml/min/100 ml forearm tissue (p<0.001) during higher dosages (25 and 50 ng/min/100 ml forearm tissue). Sodium nitroprusside (0.6 ,g/min/100 ml forearm tissue, n=6), acetylcholine (16 ,g/min/100 ml forearm tissue, n=7), nifedipine (6 pg/min/100 ml forearm tissue, n=6), and verapamil (80 ,ug/min/100 ml forearm tissue, n=6) were infused alone and in combination with ET to evaluate the interactions between ET-induced vasoconstriction and stimulation of vascular muscle cyclic GMP levels by sodium nitroprusside, release of endothelium-derived relaxing factor by acetylcholine, and blockade of voltage-operated calcium channels by nifedipine and verapamil. Neither the vasodilator nor the vasoconstrictor response to ET was influenced by sodium nitroprusside or acetylcholine. In contrast, both calcium antagonists converted ET-induced vasoconstriction (e.g., A forearm vascular resistance to ET 50 ng/min/ 100 ml forearm tissue, 151±100%o and 164±92% in verapamil and nifedipine groups, respectively) to vasodilation (-35±12% and -21±16%,p<0.05). Our results demonstrate both ET-induced vasodilation (at low dosages) and vasoconstriction (at high dosages) in resistance vessels of normal humans. Blockade of voltage-operated calcium channels prevented ETinduced vasoconstriction and unmasked the vasodilator effect of high ET dosages. In human resistance vessels, blockade of voltage-operated Ca'+ channels but not cyclic GMP-dependent vasodilation may be an effective tool to inhibit ET-induced vasoconstriction. (Circulation 1991;83:469-475)
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تاریخ انتشار 2005