Cauvin C, Weir S W, Wallnöfer A, Rüegg U
Preclinical Research, Sandoz Ltd., Basel, Switzerland.
J Cardiovasc Pharmacol. 1988;12 Suppl 5:S128-33.
The effects of noradrenaline (NA, 10(-5) M) and [arginine8]vasopressin (AVP, 10(-7) M) on tension in Ca2+-free medium and on membrane potential, and the inhibition of NA- and AVP-induced contractions by isradipine, have been compared in mesenteric resistance vessels (MRVs) from Wistar-Kyoto (WKY) rats. The release of intracellular Ca2+ by AVP contributed significantly less to its tension development than does that by NA. Nonetheless, the concentration-response curves for inhibition by isradipine of NA- and AVP-induced tonic tension were nearly identical. Similarly, these two agonists produced the same degree of membrane depolarization. In addition, both agonists were able to stimulate large contractions in vessels previously depolarized by 80 mM K+. AVP also stimulated 45Ca influx into rat cultured aortic smooth muscle cells. In contrast to the stimulation of 45Ca influx by KCl depolarization, the agonist-stimulated 45Ca influx was insensitive to inhibition by organic Ca2+ antagonists. It is concluded that Ca2+ entry through receptor-operated Ca2+-permeable channels (ROCs) may contribute to agonist-induced activation of rat aortic and MRV smooth muscle.
在来自Wistar-Kyoto（WKY）大鼠的肠系膜阻力血管（MRV）中，比较了去甲肾上腺素（NA，10⁻⁵ M）和[精氨酸⁸]血管加压素（AVP，10⁻⁷ M）对无钙培养基中张力和膜电位的影响，以及异搏定对NA和AVP诱导的收缩的抑制作用。与NA相比，AVP引起的细胞内Ca²⁺释放对其张力发展的贡献明显较小。尽管如此，异搏定对NA和AVP诱导的强直张力的抑制浓度-反应曲线几乎相同。同样，这两种激动剂产生的膜去极化程度相同。此外，两种激动剂都能够刺激先前由80 mM K⁺去极化的血管产生大的收缩。AVP还刺激了⁴⁵Ca流入大鼠培养的主动脉平滑肌细胞。与KCl去极化刺激的⁴⁵Ca流入相反，激动剂刺激的⁴⁵Ca流入对有机Ca²⁺拮抗剂的抑制不敏感。得出的结论是，通过受体操纵的Ca²⁺通透通道（ROCs）进入的Ca²⁺可能有助于激动剂诱导的大鼠主动脉和MRV平滑肌的激活。
