Hubbard J W, Buchholz R A, Keeton T K, Nathan M A
Department of Pharmacology, University of Texas Health Science Center, San Antonio 78284-7764.
Brain Res. 1987 Sep 22;421(1-2):226-34. doi: 10.1016/0006-8993(87)91292-3.
Electrolytic lesions of the parabrachial nucleus (PBN) caused significant increases in basal plasma renin activity (+433%) and basal plasma norepinephrine concentration (+98%) in conscious rats. Plasma epinephrine concentration, mean arterial pressure, heart rate, hematocrit, plasma osmolality and plasma sodium and potassium concentrations were not significantly affected by the lesions. Atenolol reduced the elevated plasma renin activity in the lesion group to a value similar to that of a control group (sham lesions or lesions in areas adjacent to the PBN). Captopril significantly lowered mean arterial pressure in the lesion group, but it had no effect on arterial pressure in the control group. Lesions of the PBN also increased the baroreflex-mediated bradycardia evoked by an abrupt elevation of arterial pressure. We propose that the PBN tonically inhibits sympathetic activity, sympathetically mediated renin release and baroreflex sensitivity.
在清醒大鼠中,臂旁核(PBN)的电解损伤导致基础血浆肾素活性显著增加(+433%)以及基础血浆去甲肾上腺素浓度显著增加(+98%)。血浆肾上腺素浓度、平均动脉压、心率、血细胞比容、血浆渗透压以及血浆钠和钾浓度未受到损伤的显著影响。阿替洛尔将损伤组升高的血浆肾素活性降低至与对照组(假损伤或PBN相邻区域的损伤)相似的值。卡托普利显著降低了损伤组的平均动脉压,但对对照组的动脉压没有影响。PBN损伤还增强了由动脉压突然升高诱发的压力感受性反射介导的心动过缓。我们提出,PBN对交感神经活动、交感神经介导的肾素释放以及压力感受性反射敏感性具有紧张性抑制作用。