Tagawa T, Imaizumi T, Endo T, Shiramoto M, Hirooka Y, Ando S, Takeshita A
Research Institute of Angiocardiology and Cardiovascular Clinic, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Clin Invest. 1993 Sep;92(3):1483-90. doi: 10.1172/JCI116726.
Arginine vasopressin (AVP) causes biphasic changes in vascular resistance in human forearms; vasoconstriction at lower doses and vasodilation at higher doses. Vasoconstriction is mediated by the V1 receptor. However, the mechanism of AVP-induced vasodilation is not known. We investigated whether AVP-induced vasodilation is mediated by nitric oxide (NO) in human forearms by examining the effects of L-arginine (a precursor of NO) and NG-monomethyl-L-arginine (L-NMMA, a blocker of NO synthase) on AVP-induced vasodilation. AVP was infused intraarterially at doses of 0.05, 0.1, 0.2, 0.5, and 1.0 ng/kg per min (n = 8). The lower doses of AVP (< or = 0.1 ng/kg per min) increased, whereas the higher doses of AVP (> or = 0.5 ng/kg per min) decreased forearm vascular resistance (FVR) (P < 0.01). Intraarterially infused L-arginine at 10 mg/min did not alter arterial pressure, baseline FVR, or heart rate. L-arginine did not alter the magnitude of AVP-induced vasoconstriction at the lower doses, but L-arginine augmented the magnitude of AVP-induced vasodilation at doses of 0.2 (P < 0.05), 0.5 (P < 0.01), and 1.0 (P < 0.05) ng/kg per min. In another group (n = 6), intraarterially infused L-NMMA (4 mumol/min for 5 min) increased baseline FVR without systemic effects, and inhibited acetylcholine-induced vasodilation (P < 0.01). L-NMMA at this dose inhibited AVP-induced vasodilation (P < 0.01) but did not affect vasoconstriction. L-arginine reversed the inhibitory effect of L-NMMA. Our results suggest that the vasodilatory effect of AVP may be mediated by NO in human forearms.
精氨酸加压素（AVP）可引起人体前臂血管阻力的双相变化；低剂量时血管收缩，高剂量时血管舒张。血管收缩由V1受体介导。然而，AVP诱导血管舒张的机制尚不清楚。我们通过研究L-精氨酸（NO的前体）和NG-单甲基-L-精氨酸（L-NMMA，一种一氧化氮合酶抑制剂）对AVP诱导的血管舒张的影响，来探究AVP诱导的血管舒张是否由一氧化氮（NO）介导。以每分钟0.05、0.1、0.2、0.5和1.0 ng/kg的剂量动脉内输注AVP（n = 8）。较低剂量的AVP（≤0.1 ng/kg每分钟）会使前臂血管阻力（FVR）增加，而较高剂量的AVP（≥0.5 ng/kg每分钟）会使FVR降低（P < 0.01）。以每分钟10 mg的剂量动脉内输注L-精氨酸不会改变动脉血压、基线FVR或心率。L-精氨酸不会改变低剂量AVP诱导的血管收缩幅度，但会增强0.2（P < 0.05）、0.5（P < 0.01）和1.0（P < 0.05）ng/kg每分钟剂量的AVP诱导的血管舒张幅度。在另一组（n = 6）中，动脉内输注L-NMMA（4 μmol/分钟，持续5分钟）会增加基线FVR且无全身影响，并抑制乙酰胆碱诱导的血管舒张（P < 0.01）。该剂量的L-NMMA抑制AVP诱导的血管舒张（P < 0.01），但不影响血管收缩。L-精氨酸可逆转L-NMMA的抑制作用。我们的结果表明，AVP的血管舒张作用可能由人体前臂中的NO介导。
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