García-Barrado M J, Sancho C, Iglesias-Osma M C, Moratinos J
Departamento de Fisiología y Farmacología, Facultad de Medicina, Universidad de Salamanca, Avda. de Alfonso X El Sabio, s/n, 37007 Salamanca, Spain.
Eur J Pharmacol. 2001 Mar 9;415(1):105-15. doi: 10.1016/s0014-2999(01)00808-1.
Verapamil (0.17 microg kg(-1) min(-1) intravenous, i.v.) but not elgodipine (35 ng kg(-1) min(-1)) modestly enhanced the weak blood glucose increase induced by the i.v. infusion of isoprenaline (0.3 microg kg(-1) min(-1)) in conscious rabbits. However, elgodipine but not verapamil suppressed the increase in circulating insulin evoked by the agonist. Both drugs enhanced the rise in plasma lactate mediated by isoprenaline but only elgodipine potentiated the lipolytic effect of the agonist. In isolated islets elgodipine (10(-6) M) blocked forskolin (10(-6) M)-induced insulin release. However, in rabbit adipocytes elgodipine potentiated both glycerol release and cAMP accumulation induced by isoprenaline (10(-8)-10(-6) M). Excess K(+) (40-60 mM) did not alter basal lipolysis or the response to isoprenaline in either rabbit or mouse adipocytes. Therefore, Ca2+ influx through L-type Ca2+ channels does not seem to play a significant role in the lipolytic effect of isoprenaline. Metabolic alterations found with Ca2+ channel antagonists were of minor intensity and probably devoid of pathological implications.
维拉帕米(静脉注射0.17微克/千克/分钟)而非依高地平(35纳克/千克/分钟)能适度增强静脉输注异丙肾上腺素(0.3微克/千克/分钟)在清醒兔体内引起的微弱血糖升高。然而,依高地平而非维拉帕米能抑制激动剂引起的循环胰岛素升高。两种药物均增强了异丙肾上腺素介导的血浆乳酸升高,但只有依高地平增强了激动剂的脂解作用。在分离的胰岛中,依高地平(10⁻⁶摩尔/升)可阻断福斯可林(10⁻⁶摩尔/升)诱导的胰岛素释放。然而,在兔脂肪细胞中,依高地平增强了异丙肾上腺素(10⁻⁸ - 10⁻⁶摩尔/升)诱导的甘油释放和环磷酸腺苷积累。过量钾离子(40 - 60毫摩尔/升)对兔或小鼠脂肪细胞的基础脂解或对异丙肾上腺素的反应均无影响。因此,通过L型钙通道的钙离子内流似乎在异丙肾上腺素的脂解作用中不起重要作用。钙通道拮抗剂引起的代谢改变强度较小,可能无病理意义。