Sabouni M H, Hargittai P T, Lieberman E M, Mustafa S J
Department of Pharmacology, School of Medicine, East Carolina University, Greenville, North Carolina 27858-4354.
Am J Physiol. 1989 Nov;257(5 Pt 2):H1750-2. doi: 10.1152/ajpheart.1989.257.5.H1750.
The effects of adenosine and its analogues, 5'-N-ethyl-carboxamidoadenosine (NECA) and 2-chloroadenosine (CAD), were studied on resting membrane potential of bovine coronary artery. The resting membrane potential averaged -51 +/- 1 mV. KCl (50 mM) caused a significant decrease of the resting membrane potential (-30 +/- 1 mV). In separate series of experiments suffusion of the arterial strips with adenosine, NECA, or CAD, at concentrations of 10(-5)M, produced significant increases in resting membrane potential (-68 +/- 1, -80 +/- 2, and -88 +/- 4 mV, respectively). The hyperpolarizing responses to adenosine, NECA, and CAD appeared to have been mediated by an adenosine receptor, since they were blocked by the adenosine receptor antagonist, 8-phenyltheophylline (10(-5) M). The data suggest that activation of an adenosine receptor can result in hyperpolarization of coronary smooth muscle cells.
研究了腺苷及其类似物5'-N-乙基-羧基酰胺腺苷(NECA)和2-氯腺苷(CAD)对牛冠状动脉静息膜电位的影响。静息膜电位平均为-51±1mV。50mM的KCl可使静息膜电位显著降低(-30±1mV)。在单独的一系列实验中,用浓度为10^(-5)M的腺苷、NECA或CAD灌注动脉条,可使静息膜电位显著升高(分别为-68±1、-80±2和-88±4mV)。对腺苷、NECA和CAD的超极化反应似乎是由腺苷受体介导的,因为它们被腺苷受体拮抗剂8-苯基茶碱(10^(-5)M)阻断。数据表明,腺苷受体的激活可导致冠状动脉平滑肌细胞超极化。