Gutkind J S, Kazanietz M G, Armando I, Puyó A, Enero M A
Cátedra de Farmacología, Facultad de Farmacia y Bioquímica, UBA, Argentina.
J Cardiovasc Pharmacol. 1989 May;13(5):793-8.
Short-term treatment with clenbuterol [0.6 mg/kg-1 subcutaneously (s.c.) daily] produces a pressor effect in stressed rats after a period of immobilization (40 min). The stress applied markedly increases the plasma concentrations of norepinephrine (NE) and epinephrine. After bilateral adrenal demedullation, the increased levels of catecholamines and the hypertensive response obtained after clenbuterol treatment in the stressed animals were reduced to the values of the control rats. Clenbuterol treatment produced desensitization of the beta 2-adrenoceptor-mediated effect and thus reduced the vasodilator response induced by isoproterenol and increased the vasoconstriction produced by epinephrine but not that caused by NE. This desensitization may be responsible for the hypertensive response after clenbuterol treatment in stressed animals which is attenuated after adrenal demedullation. In conclusion, our results provide evidence that clenbuterol treatment induces pressor effect in normotensive animals under stress.
在应激大鼠中,经40分钟固定后,每日皮下注射克仑特罗[0.6毫克/千克]进行短期治疗会产生升压作用。施加的应激显著增加了去甲肾上腺素(NE)和肾上腺素的血浆浓度。双侧肾上腺髓质切除后,应激动物经克仑特罗治疗后儿茶酚胺水平的升高及高血压反应降低至对照大鼠的值。克仑特罗治疗导致β2 -肾上腺素能受体介导的效应脱敏,从而降低了异丙肾上腺素诱导的血管舒张反应,并增加了肾上腺素产生的血管收缩,但不增加NE引起的血管收缩。这种脱敏可能是应激动物经克仑特罗治疗后出现高血压反应的原因,而肾上腺髓质切除后该反应减弱。总之,我们的结果提供了证据表明克仑特罗治疗在应激状态下的正常血压动物中诱导升压作用。