Goldberg M T, Triggle C R
Can J Physiol Pharmacol. 1978 Dec;56(6):1072-5. doi: 10.1139/y78-174.
Spontaneously hypertensive rats (SHR) treated in utero with a low dose, and from weaning with 6 mg/kg per day of oral timolol, a noncardioselective beta-adrenergic blocker, did not develop hypertension. Isolated aortic rings from these animals showed increased reactivity to raised extracellular K+, when compared with tissues from timolol-treated Kyoto-Wistar (WKY) control rats. The normotensive SHR aorta also showed significant responsiveness to H+ and to high Ca2+ concentrations without previously depolarizing the tissue with high K+. These observations suggest that the increased reactivity seen in vascular smooth muscle from this animal does not develop secondary to elevated peripheral resistance and subsequent hypertrophy, and that the initiation of hypertension in this animal may be related to a membrane defect and (or) cellular defect which results in a facilitation of Ca2+ availability for the contractile proteins of the SHR vascular smooth muscle cell.
在子宫内用低剂量治疗，并从断奶开始每天口服6毫克/千克的噻吗洛尔（一种非选择性β-肾上腺素能阻滞剂）的自发性高血压大鼠（SHR）未发生高血压。与用噻吗洛尔治疗的京都-威斯塔大鼠（WKY）对照大鼠的组织相比，这些动物的离体主动脉环对细胞外钾离子升高的反应性增加。正常血压的SHR主动脉对H+和高Ca2+浓度也表现出显著反应，而无需先用高钾使组织去极化。这些观察结果表明，该动物血管平滑肌中观察到的反应性增加并非继发于外周阻力升高和随后的肥大，并且该动物高血压的起始可能与膜缺陷和（或）细胞缺陷有关，这导致SHR血管平滑肌细胞收缩蛋白的Ca2+可用性增加。
