Loutzenhiser R, van Breemen C
Am J Physiol. 1981 Nov;241(5):C243-9. doi: 10.1152/ajpcell.1981.241.5.C243.
The effects of a stable analogue of PGH2 on 45Ca fluxes and tension were studied in the isolated rabbit aorta. U-44069 produced maximal tension responses at a concentration of 10(-7) M. The analogue increased smooth muscle Ca2+ content and increased the unidirectional 45Ca influx. U-44069 also induced contractions of reduced magnitude in the absence of external Ca2+ and caused a transient stimulation of 45Ca efflux, suggesting that the analogue releases intracellularly bound Ca2+. Both the contractile response in CA2+-free media and the stimulation of 45Ca efflux were greatly attenuated by prior exposure to norepinephrine. The analogue-induced contractions in Ca2+-free media were also prevented by prior exposure to histamine but not angiotensin II. D-600 completely blocked the U-44069-induced gain in calcium content (IC50 = 10(-6) M) but inhibited the contractile response by only 40%. It was concluded that the PGH2 analogue activates rabbit aorta by activating a CA2+ influx pathway and releasing a fraction of the intracellular Ca2+ pool that is sensitive to norepinephrine and other agonists.
在离体兔主动脉中研究了PGH2的一种稳定类似物对45Ca通量和张力的影响。U - 44069在浓度为10(-7) M时产生最大张力反应。该类似物增加了平滑肌Ca2+含量，并增加了单向45Ca内流。U - 44069在无细胞外Ca2+时也诱导幅度减小的收缩，并引起45Ca外流的短暂刺激，提示该类似物释放细胞内结合的Ca2+。在无Ca2+的培养基中，收缩反应和45Ca外流的刺激均因预先暴露于去甲肾上腺素而大大减弱。预先暴露于组胺可防止在无Ca2+培养基中类似物诱导的收缩，但预先暴露于血管紧张素II则不能。D - 600完全阻断了U - 44069诱导的钙含量增加(IC50 = 10(-6) M)，但仅抑制了40%的收缩反应。得出的结论是，PGH2类似物通过激活Ca2+内流途径并释放一部分对去甲肾上腺素和其他激动剂敏感的细胞内Ca2+池来激活兔主动脉。
