Lefer A M, Whitney C C, Hock C E
Pharmacology. 1986;32(4):181-9. doi: 10.1159/000138168.
The purported calcium agonist BAY k 8644 was tested as a pressor agent in pentobarbital anesthetized and conscious Sprague-Dawley rats. A dose of 10 micrograms/kg increased mean arterial blood pressure (MABP) by 47 +/- 3 mm Hg in anesthetized and 39 +/- 3 mm Hg in conscious rats. The calcium channel blockers nitrendipine or nisoldipine (180 micrograms/kg/h) blocked 62-84% of the pressor response of BAY k 8644 (p less than 0.001 from control responses). The alpha-adrenergic receptor antagonist phentolamine (400 micrograms/kg) failed to alter the Bay k 8644 induced pressor response either in the conscious or anesthetized state. Moreover, the thromboxane receptor antagonist, SQ-29,548 and the leukotriene D4 and E4 receptor antagonist LY-171,883 at doses that markedly block thromboxanes or leukotrienes, respectively, had no effect on the BAY k 8644 induced pressor response. Neither the angiotensin II receptor antagonist, saralasin nor an arginine vasopressin antagonist (AVP-A) modify the BAY k 8644 induced pressor response. Thus, BAY k 8644 appears to directly increase MABP in the rat by activation of calcium influx into vascular smooth muscle and/or cardiac muscle cells, probably without the action of any common secondary vasoconstrictor mediator.
在戊巴比妥麻醉和清醒的斯普拉格-道利大鼠中，对所谓的钙激动剂BAY k 8644作为升压剂进行了测试。剂量为10微克/千克时，在麻醉大鼠中平均动脉血压（MABP）升高47±3毫米汞柱，在清醒大鼠中升高39±3毫米汞柱。钙通道阻滞剂尼群地平或尼索地平（180微克/千克/小时）可阻断BAY k 8644升压反应的62%-84%（与对照反应相比，p<0.001）。α-肾上腺素能受体拮抗剂酚妥拉明（400微克/千克）在清醒或麻醉状态下均未能改变BAY k 8644诱导的升压反应。此外，血栓素受体拮抗剂SQ-29548以及白三烯D4和E4受体拮抗剂LY-171883，分别以能显著阻断血栓素或白三烯的剂量给药，对BAY k 8644诱导的升压反应均无影响。血管紧张素II受体拮抗剂沙拉新和精氨酸加压素拮抗剂（AVP-A）均未改变BAY k 8644诱导的升压反应。因此，BAY k 8644似乎通过激活钙流入血管平滑肌和/或心肌细胞直接增加大鼠的MABP，可能无需任何常见的继发性血管收缩介质的作用。
