Hosono M, Hiruma T, Watanabe K, Hayashi Y, Ohnishi H, Takata Y, Kato H
Pharmaceuticals Research Laboratories, Fujirebio Inc., Tokyo, Japan.
Jpn J Pharmacol. 1995 Oct;69(2):119-25. doi: 10.1254/jjp.69.119.
We investigated the effect of cilnidipine on cardiovascular and neuroendocrine responses to acute cold stress in conscious and unrestrained or moderately restrained spontaneously hypertensive rats (SHRs). Acute cold stress significantly increased mean blood pressure without marked change in heart rate. The acute cold stress-induced elevation in blood pressure was almost abolished by 1 mg/kg, p.o. of prazosin. The cold stress also elevated plasma norepinephrine and epinephrine levels. Cilnidipine at 3 mg/kg, p.o. significantly inhibited the pressor response to acute cold stress. Although 3 mg/kg, p.o. of nifedipine, nicardipine or manidipine lowered mean blood pressure to a similar extent as cilnidipine, none of these three drugs affected the pressor response. Cilnidipine also reduced the cold stress-induced increment in plasma norepinephrine but not the epinephrine level. These findings suggest that acute cold stress may induce the elevation in blood pressure due to an enhanced activation of the sympathoadrenal system in SHRs and that cilnidipine may suppress the pressor response by inhibiting the sympathetic nerve activity.
我们研究了西尼地平对清醒、未束缚或适度束缚的自发性高血压大鼠(SHR)急性冷应激时心血管和神经内分泌反应的影响。急性冷应激显著升高平均血压,而心率无明显变化。1mg/kg口服哌唑嗪几乎可消除急性冷应激诱导的血压升高。冷应激还会升高血浆去甲肾上腺素和肾上腺素水平。3mg/kg口服西尼地平可显著抑制对急性冷应激的升压反应。尽管3mg/kg口服硝苯地平、尼卡地平或马尼地平使平均血压降低程度与西尼地平相似,但这三种药物均未影响升压反应。西尼地平还可降低冷应激诱导的血浆去甲肾上腺素升高,但对肾上腺素水平无影响。这些发现表明,急性冷应激可能通过增强SHR交感肾上腺系统的激活而导致血压升高,且西尼地平可能通过抑制交感神经活动来抑制升压反应。