McLaren G J, Kennedy C, Sneddon P
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, Scotland, UK.
Eur J Pharmacol. 1995 Apr 13;277(1):57-61. doi: 10.1016/0014-2999(95)00065-s.
Intracellular microelectrode recording was used to examine the effects of suramin, a P2-purinoceptor antagonist, on the electrical responses evoked by sympathetic nerve stimulation in the rat isolated tail artery. Field stimulation (10 or 20 pulses at 0.5, 1 and 2 Hz) evoked a biphasic electrical response, consisting of fast, transient excitatory junctional potentials (e.j.p.s) and a slow, prolonged depolarisation. Suramin (100 microM) abolished the e.j.p.s and significantly increased the amplitude of the slow depolarisation at all frequencies. In contrast, phentolamine (2 microM) abolished the slow depolarisation, but had no effect on the magnitude of e.j.p.s. Neither drug altered the resting membrane potential of cells. The ability of suramin to inhibit e.j.p.s in rat tail artery is consistent with the proposal that it is a P2X-purinoceptor antagonist and supports a role for ATP as an excitatory cotransmitter from the sympathetic nerves innervating this tissue. Suramin is also able to increase the alpha-adrenoceptor-mediated slow depolarisation by an unknown mechanism.
采用细胞内微电极记录法，研究P2嘌呤受体拮抗剂苏拉明对大鼠离体尾动脉交感神经刺激诱发的电反应的影响。场刺激（0.5、1和2Hz频率下10或20个脉冲）诱发双相电反应，包括快速、短暂的兴奋性突触后电位（e.j.p.s）和缓慢、持久的去极化。苏拉明（100μM）消除了e.j.p.s，并在所有频率下显著增加了缓慢去极化的幅度。相比之下，酚妥拉明（2μM）消除了缓慢去极化，但对e.j.p.s的幅度没有影响。两种药物均未改变细胞的静息膜电位。苏拉明抑制大鼠尾动脉e.j.p.s的能力与它是一种P2X嘌呤受体拮抗剂的观点一致，并支持ATP作为支配该组织的交感神经的兴奋性共递质的作用。苏拉明还能够通过未知机制增加α-肾上腺素能受体介导的缓慢去极化。
