ON THE VASCULAR INOTROPIC ACTION OF 1,25-(OH)2 VITAMIN-D3

ON THE VASCULAR INOTROPIC ACTION OF 1,25-(OH)2 VITAMIN-D3
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DOI:
10.1093/ajh/6.5.388
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发表时间:
1993-05-01
影响因子:
3.2
通讯作者:
XUE, H
XUE, H
中科院分区:
医学3区
文献类型:
--
作者:
BUKOSKI, RD;XUE, H

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我们实验室以前的工作表明,在3天内向大鼠注射1,25-(OH)2维生素D3(1,25-vitD)可增加随后分离的阻力动脉的力产生能力。为了更好地了解这种血管变力作用的机制,我们研究了其发展的时间过程和Ca 2+相关的作用机制。从12周龄的雄性自发性高血压大鼠(SHR)中分离肠系膜阻力动脉,在单次注射1,25-维生素D(20 ng/100 g)或媒介物后6和24 h以及在连续3天和7天注射1,25-维生素D(20 ng/100 g)或媒介物后24 h。血清1,25-维生素D增加近三倍,在6小时,但不是在以后的时间。血清总钙和离子钙在任何时间点均不受影响。在6和24小时未检测到收缩力产生的变化,但在1,25-vitD治疗3天和7天后观察到对去甲肾上腺素和精氨酸加压素的主动应激反应显著增加。在任何时间点均未观察到对任一激动剂敏感性的影响。为了确定1,25-维生素D的血管变力作用是否会转化为血压的变化,在4周的时间内,每天给11周龄的雄性Wistar大鼠注射1,25-维生素D(20 ng/100 g),并测量血压和体重。虽然两组的体重在任何时间点都没有差异,但1,25-vitD组与对照组相比,收缩压在7天内升高,并在观察期间继续升高。我们的结论是,1,25-维生素D的血管变力作用呈现出与基因组机制相一致的时间过程,而不是快速的非核作用,并且该激素增加血压正常大鼠的血压。
Previous work from our laboratory showed that injection of 1,25-(OH)2 vitamin D3 (1,25-vitD) into the rat over a 3-day period increases force generating capacity of subsequently isolated resistance arteries. To better understand the mechanism of this vascular inotropic action, we examined the time course of its development and Ca2+-associated mechanism of action. Mesenteric resistance arteries were isolated from 12-week-old male spontaneously hypertensive rats (SHR) 6 and 24 h after a single injection and 24 h after three and seven consecutive days of injection of 1,25-vitD (20 ng/100 g) or vehicle. Serum 1,25-vitD was increased nearly threefold at 6 h, but not at later times. Serum total and ionized Ca2+ were not affected at any time point. No changes in contractile force generation were detected at 6 and 24 h, but a significant increase in the active stress response to norepinephrine and arginine vasopressin was observed after both 3 and 7 days of 1,25-vitD treatment. No effect on sensitivity to either agonist was observed at any time point. To determine whether the vascular inotropic effects of 1,25-vitD might translate into changes in blood pressure, 11-week-old male Wistar rats were given daily injections of 1,25-vitD (20 ng/100 g) over a 4-week period, and blood pressure and body weight were measured. While body weight did not differ at any time point in the two groups, systolic blood pressure was elevated in the 1,25-vitD group v control by 7 days, and continued to be elevated over the period of observation. We conclude that the vascular inotropic action of 1,25-vitD presents with a time course that is consistent with a genomic mechanism rather than a rapid, nonnuclear action, and that the hormone increases blood pressure in the normotensive rat.