一氧化氮介导的心房利钠肽对健康人前臂血管的舒张作用。

Nitric oxide-mediated vasodilatory effect of atrial natriuretic peptide in forearm vessels of healthy humans.

作者信息

Sugamori Takashi, Ishibashi Yutaka, Shimada Toshio, Sakane Takeshi, Takahashi Nobuyuki, Ohata Shuzo, Kodani Nobuhiro, Kunizawa Yoshitsugu, Inoue Shin-ichi, Ohta Yoko, Nakamura Ko, Shimizu Hiromi, Katoh Harumi, Murakami Yo

机构信息

The Fourth Department of Internal Medicine, Shimane Medical University, Izumo, Japan.

出版信息

Clin Exp Pharmacol Physiol. 2002 Jan-Feb;29(1-2):92-7. doi: 10.1046/j.1440-1681.2002.03597.x.

DOI:10.1046/j.1440-1681.2002.03597.x

PMID:11906465

Abstract

The aim of the present study was to determine whether the vasorelaxant effect of atrial natriuretic peptide (ANP) is, in part, endothelium dependent in humans. 2. We used veno-occlusive plethysmography to measure forearm blood flow (FBF) during intra-arterial infusions of ANP (4, 8, 16, 32 pmol/min per dL forearm tissue volume) before and after the inhibition of nitric oxide (NO) synthesis by N(G)-monomethyl-L-arginine (L-NMMA; 100 micromol) in seven normal healthy subjects. 3. Atrial natriuretic peptide caused a dose-dependent increase in FBF both before and after L-NMMA and significantly reduced the plasma concentration of angiotensin (Ang) II. Administration of L-NMMA significantly diminished the increase in FBF in response to ANP infusion (P < 0.05). 4. These results suggest that the forearm vasodilative response to ANP is modulated, in part, by an endothelium-derived NO-mediated mechanism associated with a decrease in AngII caused by ANP.

摘要

本研究的目的是确定在人类中，心房利钠肽（ANP）的血管舒张作用是否部分依赖于内皮。2. 我们使用静脉闭塞体积描记法，在7名正常健康受试者中，通过N(G)-单甲基-L-精氨酸（L-NMMA；100微摩尔）抑制一氧化氮（NO）合成前后，测量动脉内输注ANP（每分升前臂组织体积4、8、16、32皮摩尔/分钟）期间的前臂血流量（FBF）。3. 心房利钠肽在L-NMMA给药前后均引起FBF剂量依赖性增加，并显著降低血浆血管紧张素（Ang）II浓度。给予L-NMMA显著减弱了对ANP输注的FBF增加反应（P<0.05）。4. 这些结果表明，前臂对ANP的血管舒张反应部分受内皮衍生的NO介导机制调节，该机制与ANP引起的AngII降低有关。