Increased vascular reactivity to Bay K 8644 in genetic hypertension.
Increased vascular reactivity to Bay K 8644 in genetic hypertension.
复制标题
遗传性高血压患者对 Bay K 8644 的血管反应性增加。
作者：
Bruner,CA;Webb,RC
这些实验比较了易卒中的自发性高血压大鼠（SHRSP）和血压正常的Wistar-Kyoto大鼠（WKY）平滑肌中的电位操纵性钙通道功能。将成年雄性SHRSP和WKY大鼠颈动脉条悬置在组织浴中进行等长力记录。收缩力表示为对100 mmol/l KCl的反应百分比。与WKY大鼠血管条（ED 50 = 37 mmol/l）相比，SHRSP血管条对KCl（ED 50 = 25 mmol/l）更敏感。钙通道激动剂Bay K 8644（2.8 × 10- 10至2.8 × 10- 7 mol/l）对SHRSP的颈动脉条产生强直性收缩（对100 mmol/l KCl的收缩反应的34%），但对WKY大鼠的颈动脉条则没有。血管条在1.8或6 × 10 ~（-10）mmol/l去甲肾上腺素中孵育，均不改变对BayK 8644的最大收缩反应。在12 mmol/l KCl中，对Bay K 8644的最大收缩反应在SHRSP（71%）和WKY大鼠（25%）中均增加。在18 mmol/l KCl中，两种品系对Bay K 8644的最大收缩反应相似（SHRSP = 73%，WKY = 76%）。去除内皮细胞并没有显着影响收缩反应湾K 8644在任一品系的大鼠。SHRSP和WKY大鼠颈动脉对钙离子载体A23187的收缩反应或硝苯地平诱导的钾激活血管舒张反应无差异。总之，这些结果表明，电压操纵的钙通道功能的差异可能是SHRSP血管平滑肌对去极化刺激的敏感性增加的基础。
These experiments compared potential-operated calcium channel function in smooth muscle from stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). Carotid artery strips from adult male SHRSP and WKY rats were suspended in tissue baths for isometric force recording. Contractile force was expressed as percent of response to 100 mmol/l KCl. Vascular strips from SHRSP were more sensitive to KCl (ED50= 25 mmol/l) compared to strips from WKY rats (ED50= 37 mmol/l). The calcium channel agonist Bay K 8644 (2.8 × 10–10to 2.8 × 10–7mol/l) produced tonic contractions in carotid artery strips from SHRSP (34% of the contractile response to 100 mmol/l KCl) but not in those from WKY rats. Incubation of vascular strips in 1.8 or 6 × 10–10mmol/l norepinephrine did not alter the maximal contractile response to Bay K 8644 in either strain of rats. In 12 mmol/l KCl, the maximal contractile response to Bay K 8644 was increased in both SHRSP (71%) and WKY rats (25%). In 18 mmol/l KCl, maximal contractile responses to Bay K 8644 in the two strains were similar (SHRSP = 73%, WKY = 76%). Removal of the endothelium did not significantly affect contractile responses to Bay K 8644 in either strain of rats. There were no differences in contractile responses to the calcium ionophore A23187 or in nifedipine-induced relaxation of potassium-activated vessels between carotid arteries from SHRSP and WKY rats. In summary, these results suggest that a difference in voltage-operated calcium channel function may underlie the increased sensitivity of SHRSP vascular smooth muscle to depolarizing stimuli.