Rascher W, Meffle H, Gross F
Am J Physiol. 1985 Jul;249(1 Pt 2):H29-33. doi: 10.1152/ajpheart.1985.249.1.H29.
By means of a specific antagonist [d(CH2)5AVP] of the vasoconstrictor activity of arginine vasopressin (AVP), we studied whether the vasoconstrictor effect of AVP contributed to the blood pressure control during water deprivation in conscious rats. After 24 h of dehydration plasma AVP rose from 3.5 +/- 0.5 to 11.2 +/- 2.0 fmol/ml. Intravenous injection of 5 micrograms/kg d(CH2)5AVP reduced total peripheral resistance. Since cardiac output rose simultaneously, mean arterial blood pressure remained unchanged. In rats with sinoaortic deafferentation (SAD) 4 wk before water deprivation, d(CH2)5AVP caused a reduction of total peripheral resistance and of mean arterial pressure, whereas cardiac output remained unchanged. Consequently, mean arterial pressure fell. No hemodynamic changes were observed in hydrated control rats with and without SAD. It is concluded that the vasoconstrictor activity of AVP plays an important role in maintaining blood pressure during water deprivation in conscious rats. After AVP blockade, arterial pressure fell only in SAD rats as intact rats maintain arterial pressure via acute increase cardiac output.
通过使用精氨酸加压素（AVP）血管收缩活性的特异性拮抗剂[d(CH2)5AVP]，我们研究了AVP的血管收缩作用是否有助于清醒大鼠缺水期间的血压控制。脱水24小时后，血浆AVP从3.5±0.5飞升至11.2±2.0飞摩尔/毫升。静脉注射5微克/千克的d(CH2)5AVP可降低总外周阻力。由于心输出量同时增加，平均动脉血压保持不变。在缺水前4周进行了去窦主动脉神经支配（SAD）的大鼠中，d(CH2)5AVP导致总外周阻力和平均动脉血压降低，而心输出量保持不变。因此，平均动脉血压下降。在有或没有SAD的水合对照大鼠中未观察到血流动力学变化。结论是，AVP的血管收缩活性在清醒大鼠缺水期间维持血压方面起重要作用。AVP阻断后，仅SAD大鼠的动脉血压下降，因为完整大鼠通过急性增加心输出量来维持动脉血压。
