Khoyi M A, Bjur R A, Westfall D P
Department of Pharmacology, University of Nevada School of Medicine, Reno 89557.
Am J Physiol. 1993 Nov;265(5 Pt 1):C1325-31. doi: 10.1152/ajpcell.1993.265.5.C1325.
Exposure of the rabbit abdominal aorta to the combination of high K+ and norepinephrine resulted in a time-dependent increase in the rate of 45Ca influx and 45Ca and 22Na content over that observed after stimulation with either K+ or norepinephrine alone. The increase in 45Ca influx, but not the increase in 22Na content, was extracellular Ca2+ (Cao2+) dependent. This time-dependent increase in 45Ca influx was prevented by incubating the tissue in Na(+)-free medium. Nifedipine inhibited both the initial depolarization-induced 45Ca influx and time-dependent increase in 45Ca influx and 22Na content. The effect of nifedipine on time-dependent fluxes was prevented by ouabain. Phorbol dibutyrate mimicked the effects of norepinephrine on 22Na retention and 45Ca fluxes. The effects of phorbol dibutyrate and norepinephrine were not additive. It is concluded that, in rabbit abdominal aorta, norepinephrine plus K+ causes 22Na retention (possibly through inhibition of the sodium pump) and a Cao(2+)- and intracellular Na+ (Nai+)-dependent increase in 45Ca influx. This latter effect is possibly the result of increased Nai(+)-Cao2+ exchange.
将兔腹主动脉暴露于高钾和去甲肾上腺素的组合下,与单独用钾离子或去甲肾上腺素刺激后相比,45Ca内流速率以及45Ca和22Na含量随时间增加。45Ca内流的增加而非22Na含量的增加依赖于细胞外钙离子(Cao2+)。通过在无钠培养基中孵育组织可阻止这种45Ca内流随时间的增加。硝苯地平抑制初始去极化诱导的45Ca内流以及45Ca内流和22Na含量随时间的增加。哇巴因可阻止硝苯地平对随时间变化的通量的影响。佛波醇二丁酸酯模拟了去甲肾上腺素对22Na潴留和45Ca通量的影响。佛波醇二丁酸酯和去甲肾上腺素的作用并非相加的。结论是,在兔腹主动脉中,去甲肾上腺素加钾离子导致22Na潴留(可能通过抑制钠泵)以及依赖于Cao(2+)和细胞内钠离子(Nai+)的45Ca内流增加。后一种效应可能是Nai(+)-Cao2+交换增加的结果。