α-人心房利钠肽对豚鼠离体心脏的作用。

Effects of alpha-human atrial natriuretic peptide in guinea-pig isolated heart.

作者信息

Di Nardo P, Pafi M, Bartoli M, Minieri M, Bellegrandi F, Raimondi G, Peruzzi G, Tallarida G

机构信息

Department of Internal Medicine, University of Rome Tor Vergata, Italy.

出版信息

Int J Cardiol. 1993 Jul 15;40(3):211-20. doi: 10.1016/0167-5273(93)90003-y.

DOI:10.1016/0167-5273(93)90003-y

PMID:8225656

Abstract

The aim of the present investigation has been to ascertain whether or not atrial natriuretic peptides (ANP) can exert a direct effect on myocardial contractility. Alpha-human ANP (alpha-hANP) concentrations ranging from 1 pM to 50 nM have been used to perfuse guinea-pig isolated hearts in a non-recirculating Langendorff apparatus. A dual concentration-related effect has been induced by alpha-hANP on myocardial function. A maximal increase of +LV dP/dtmax (+56%; P < 0.001) has been observed when guinea-pig hearts were perfused with 100 pM alpha-hANP, whereas a 25% decrease (P < 0.01) occurred with 50 nM alpha-hANP. Similar effects have also been induced by alpha-hANP on the coronary flow rate (CFR). A significant CFR increase (maximal at 10 pM alpha-hANP) was induced by picomolar concentrations of alpha-hANP, whereas a progressive decrease, which was maximal (-28%; P < 0.01) at 50 nM alpha-hANP, was observed with nanomolar concentrations of the peptide. No effects have been observed on heart rate. These results suggest that ANP has direct effects on both vascular and myocardial muscle cells. Coronary vasoconstriction induced by nanomolar concentrations of ANP can contribute to the cardiodepression, whereas ANP in picomolar concentrations can induce a coronary vasodilation which is not coupled with the enhanced myocardial contractility. The latter is the likely expression of a direct effect of the peptide on myocardial function.

摘要

本研究的目的是确定心钠素（ANP）是否能对心肌收缩力产生直接影响。在非循环Langendorff装置中，使用浓度范围为1 pM至50 nM的α-人ANP（α-hANP）灌注豚鼠离体心脏。α-hANP对心肌功能产生了双相浓度相关效应。当用100 pM的α-hANP灌注豚鼠心脏时，观察到左心室最大dp/dtmax有最大增加（+56%；P<0.001），而当使用50 nM的α-hANP时则出现25%的下降（P<0.01）。α-hANP对冠状动脉血流量（CFR）也产生了类似效应。皮摩尔浓度的α-hANP可引起CFR显著增加（在10 pM的α-hANP时最大），而当使用纳摩尔浓度的该肽时，观察到逐渐下降，在50 nM的α-hANP时下降最大（-28%；P<0.01）。未观察到对心率的影响。这些结果表明，ANP对血管和心肌细胞均有直接作用。纳摩尔浓度的ANP诱导的冠状动脉收缩可能导致心脏抑制，而皮摩尔浓度的ANP可诱导冠状动脉舒张，且这与增强的心肌收缩力无关。后者可能是该肽对心肌功能直接作用的表现。