Dong Y, Wadsworth R M
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow, UK.
J Hypertens. 1987 Dec;5(6):711-4. doi: 10.1097/00004872-198712000-00013.
Uptake of 45Ca was measured in rings of thoracic aorta from rabbits with hypertension, induced by cellophane perinephritis (Page hypertension: one-kidney, one wrap). Basal 45Ca uptake was increased significantly in the hypertensive group (sham: 100 +/- 3, hypertensive: 133 +/- 11 nmol/g wet weight, n = 6). 45Ca uptake was increased by KCl (30 mmol/l), norepinephrine (50 nmol/l) and Bay K 8644 (14 or 56 nmol/l) by the following amounts: 152, 15, 28 and 36%, respectively. Stimulated 45Ca uptake was less in hypertensive animals for all agonists. The augmenting effect of Bay K 8644 on 45Ca uptake, stimulated by norepinephrine or by KCl, was also reduced in hypertension. It is concluded that in hypertension there are alterations in the Ca regulatory process and in the properties of the Ca channel in arterial muscle.
采用玻璃纸肾周炎诱导的高血压兔（佩奇高血压：单肾单包裹）胸主动脉环，测定45Ca摄取量。高血压组基础45Ca摄取量显著增加（假手术组：100±3，高血压组：133±11 nmol/g湿重，n = 6）。氯化钾（30 mmol/L）、去甲肾上腺素（50 nmol/L）和Bay K 8644（14或56 nmol/L）使45Ca摄取量分别增加以下幅度：152%、15%、28%和36%。对于所有激动剂，高血压动物中刺激后的45Ca摄取量较少。在高血压状态下，Bay K 8644对去甲肾上腺素或氯化钾刺激的45Ca摄取量的增强作用也降低。结论是，高血压时动脉平滑肌中钙调节过程和钙通道特性发生改变。
