Attenuation of pressor responses to arginine vasopressin in right-sided congestive heart failure.
Attenuation of pressor responses to arginine vasopressin in right-sided congestive heart failure.
复制标题
右侧充血性心力衰竭患者对精氨酸加压素的升压反应减弱。
DOI：
10.1152/ajpheart.1990.258.6.h1882
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Liang,CS
中科院分区：
文献类型：
--
作者：
Stone,CK;Imai,N;Sladek,CD;Liang,CS
尽管精氨酸抗利尿激素（AVP）在心力衰竭时升高，抑制抗利尿激素能v1受体可使血压发生微小变化。为了确定V1血管收缩效应是否在心力衰竭中减弱，我们随机给11只右侧充血性心力衰竭（RHF）犬和7只假手术犬静脉注射三次增加剂量的AVP和甲氧沙明。与假手术犬相比，RHF组血浆AVP升高（21 +/- 3 pg/ml） （3.8 +/- 0.6 pg/ml）。虽然两组对甲氧沙明的降压反应相似，但AVP导致RHF犬的平均主动脉压升高幅度小于假手术犬。为了确定对AVP的压力反应差异是否由RHF中交感神经活动的反射撤回比假手术犬更大引起，我们还在这些动物用普拉唑嗪和心得安预处理后给药AVP。肾上腺素受体阻断可增强AVP的升压反应；然而，与假手术犬相比，RHF犬的平均主动脉压的增加仍然较小。与类似处理的假犬相比，肾上腺素受体阻断的RHF犬的降压反应减弱与总外周血管阻力的较小增加有关。因此，尽管AVP的降压反应被压反射激活所抵消，但AVP在心力衰竭中的降压作用减弱不能仅仅用交感神经戒断来解释。当血管加压能系统在心力衰竭中长期激活时，AVP可能发挥较小的直接血管收缩作用。
Although arginine vasopressin (AVP) is elevated in heart failure, inhibition of the vasopressinergic V1-receptor produces minimal changes in blood pressure. To determine whether the V1 vasoconstrictor effect is attenuated in heart failure, we randomly administered three increasing doses of AVP and methoxamine intravenously to 11 dogs with right-sided congestive heart failure (RHF) and 7 sham-operated dogs. Plasma AVP was elevated in RHF (21 +/- 3 pg/ml) compared with sham-operated dogs (3.8 +/- 0.6 pg/ml). While the pressor response to methoxamine was similar in the two groups, AVP caused a smaller increase in mean aortic pressure in RHF dogs than sham-operated dogs. To determine whether the difference in the pressor response to AVP was caused by greater reflex withdrawal of the sympathetic activity in RHF than sham-operated dogs, we also administered AVP after these animals had been pretreated with prazosin and propranolol. Adrenoceptor blockade exaggerated the pressor response to AVP; however, the increase in mean aortic pressure was still smaller in RHF than sham-operated dogs. The diminished pressor response in adrenoceptor-blocked RHF dogs was associated with a smaller increase in total peripheral vascular resistance compared with similarly treated sham dogs. Thus, although the pressor response to AVP was offset by baroreflex activation, the attenuated pressor effect of AVP in heart failure cannot be explained by sympathetic withdrawal alone. AVP probably exerts a smaller direct vasoconstrictor effect when the vasopressinergic system is chronically activated in heart failure.