Effect of adenosine on calcium uptake by intact and cultured vascular smooth muscle.
Effect of adenosine on calcium uptake by intact and cultured vascular smooth muscle.
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腺苷对完整和培养的血管平滑肌钙吸收的影响。
DOI：
10.1152/ajpheart.1982.242.5.h797
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Berne,RM
中科院分区：
文献类型：
--
作者：
Fenton,RA;Bruttig,SP;Rubio,R;Berne,RM
本文研究了腺苷（ADO）对血管平滑肌（VSM）细胞钙摄取的影响。此外，用其他血管活性剂进行类似的实验，以确保用培养的VSM细胞模型获得的结果的有效性。将来自大鼠主动脉的原代VSM单层在富含45 Ca的生理盐溶液（PSS）（37 ℃）中孵育30分钟，并用20 mM Ca-EGTA（4 ℃）洗涤以除去细胞外45 Ca。4.6 mM K+的钙摄取为65.3 +/- 2.4 pmol Ca/10（5）个细胞。维拉帕米（10（-6）M）或4 ℃孵育分别使该值降低27%和65%，而ADO（10（-7）M）和异丙肾上腺素（10（-6）M）分别使钙摄取增加21%和9%。细胞外K+（25 mM）升高使钙摄取增加至87.8 +/- 5.0 pmol Ca/10（5）个细胞。ADO（10（-7）M）、异丙肾上腺素（10（-6）M）和4 ℃孵育分别显著减弱了K+诱导的增加25%、19%和64%。在α-或β-肾上腺素能阻滞剂存在下，去甲肾上腺素（10（-6）M）不改变非去极化细胞的钙摄取。在存在α-和β-肾上腺素能阻滞剂的情况下，以类似的方式用猪颈动脉条进行实验。在培养基K+升高到25 mM后，钙摄取从2.3 +/-0.2 × 10 - 7 mol Ca/g湿重增加到3.0 +/- 0.1 × 10 - 7 mol Ca/g湿重。ADO（10（-6）M）对培养的VSM的~（45）Ca流出无影响。结论：ADO通过减少刺激过程中钙离子的内移来松弛VSM。在培养的细胞未部分去极化的条件下，ADO诱导的细胞钙显著升高表明这些细胞内存在增强的钙螯合。
The effect of adenosine (ADO), a potent vasodilator, on the cellular calcium uptake by vascular smooth muscle (VSM) was studied. In addition, similar experiments were conducted with other vasoactive agents to ensure the validity of results obtained with the cultured VSM cell model. Primary VSM monolayers from rat aorta were incubated for 30 min in 45Ca-enriched physiological salt solution (PSS) (37 degrees C) and washed with 20 mM Ca-EGTA (4 degrees C) to remove extracellular 45Ca. Calcium uptake with 4.6 mM K+ was 65.3 +/- 2.4 pmol Ca/10(5) cells. Verapamil (10(-6) M) or 4 degrees C incubation decreased this value 27 and 65%, respectively, whereas ADO (10(-7) M) and isoproterenol (10(-6) M) elevated calcium uptake 21 and 9%, respectively. Elevation of extracellular K+ (25 mM) increased calcium uptake to 87.8 +/- 5.0 pmol Ca/10(5) cells. ADO (10(-7) M), isoproterenol (10(-6) M), and 4 degrees C incubation significantly attenuated this K+-induced increase 25, 19, and 64%, respectively. The calcium uptake of nondepolarized cells was not changed by norepinephrine (10(-6) M) in the presence of either alpha- or beta-adrenergic blockade. Experiments were performed in a similar manner with porcine carotid artery strips in the presence of alpha- and beta-adrenergic blockade. Calcium uptake increased from 2.3 +/- 0.2 X 10(-7) to 3.0 +/- 0.1 X 10(-7) mol Ca/g wet wt after elevation of the medium K+ to 25 mM. This increase was inhibited by 10(-6) M ADO. ADO (10(-6) M) was found to have no effect on the 45Ca efflux from cultured VSM. It is concluded that ADO relaxes VSM by reducing the inward movement of calcium during stimulation. The significant ADO-induced elevation of cellular calcium under conditions when cultured cells were not partially depolarized suggests the existence of an enhanced calcium sequestration within these cells.