Cserep G, Abraham G, Tolins J P, Simon G
Department of Medicine, VA Medical Center, Minneapolis, Minnesota 55417, USA.
Am J Hypertens. 1996 Apr;9(4 Pt 1):385-92. doi: 10.1016/0895-7061(95)00398-3.
Administered in small doses, angiotensin II (ANG II) potentiates its own pressor responses (autopotentiation). In the present study, we investigated whether potentiation of vasoconstrictor responses in the mesenteric and renal circulation accounted for the autopotentiation of pressor responses. Male Sprague-Dawley rats, 350 to 400 g, were infused with 200 ng/kg/min ANG II intraperitoneally for 7 to 10 days. Control rats were fitted with an osmotic minipump containing vehicle only. Vascular responses to ANG II, norepinephrine (NE), arginine vasopressin (AVP) and nerve stimulation were measured in the mesenteric and renal circulation of rats. In ANG II-treated rats: 1) tail systolic BP was 4 mm Hg higher than in controls (P = NS); 2) mesenteric vascular responses to ANG II (P < .002) and nerve stimulation (P = .03) were increased, and those to NE and AVP were unchanged; and 3) renal vascular responses to nerve stimulation were reduced (P < .02), and those to ANG II, NE, and AVP were unchanged. Thus, we demonstrated autopotentiation of vascular responses to ANG II in the mesenteric, but not the renal circulation. An interaction between ANG II and sympathetic activity may explain these differences in regional vascular responses. Regional hemodynamic measurements may provide important clues to pathogenetic mechanisms in hypertension.
小剂量注射时,血管紧张素II(ANG II)可增强其自身的升压反应(自身增强作用)。在本研究中,我们调查了肠系膜和肾循环中血管收缩反应的增强是否可解释升压反应的自身增强作用。对体重350至400克的雄性Sprague-Dawley大鼠腹腔内注射200纳克/千克/分钟的ANG II,持续7至10天。对照大鼠安装仅含赋形剂的渗透微型泵。测量大鼠肠系膜和肾循环中对ANG II、去甲肾上腺素(NE)、精氨酸加压素(AVP)和神经刺激的血管反应。在接受ANG II治疗的大鼠中:1)尾收缩压比对照大鼠高4毫米汞柱(P =无显著性差异);2)肠系膜血管对ANG II(P <.002)和神经刺激(P =.03)的反应增强,对NE和AVP的反应未改变;3)肾血管对神经刺激的反应降低(P <.02),对ANG II、NE和AVP的反应未改变。因此,我们证明了肠系膜而非肾循环中血管对ANG II反应的自身增强作用。ANG II与交感神经活动之间的相互作用可能解释了这些区域血管反应的差异。区域血流动力学测量可能为高血压的发病机制提供重要线索。