Evidence for a central role for vasopressin in cardiovascular regulation.
Evidence for a central role for vasopressin in cardiovascular regulation.
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加压素在心血管调节中发挥核心作用的证据。
DOI：
10.1152/ajpheart.1983.244.6.h852
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Brody,MJ
中科院分区：
文献类型：
--
作者：
Berecek,KH;Webb,RL;Brody,MJ
中枢加压素（VP）可调节参与心血管调节的特定神经系统的功能活动。为了验证这一假设，我们比较了Brattleboro尿崩症纯合子大鼠（DI）、尿崩症杂合子大鼠（DI-HZ）和正常Long-Evans大鼠（LE）对第三脑室前腹区（AV 3V）电刺激的心血管（CV）反应。我们还研究了外周和侧脑室（ivt）治疗的DI大鼠与VP和治疗LE大鼠与VP的降压阻断剂对AV 3V刺激的心血管反应的影响。在麻醉LE大鼠中刺激AV 3V区域产生肾（RVR）和肠系膜血管阻力（MVR）的频率依赖性增加，后躯血管阻力（HQVR）降低，以及动脉压（AP）和心率（HR）降低。DI和DI-HZ大鼠的AP和HR下降幅度显著更大，RVR、MVR和HQVR变化较小。DI大鼠血管收缩的不足似乎是中枢介导的，因为LE和DI大鼠对外周给药苯肾上腺素和神经刺激的血管反应相当。用VP外周治疗DI大鼠改善了对AV 3V刺激的CV反应。当给予DI静脉输注VP时，对AV 3V刺激的CV反应得到更大的改善。最后，静脉注射抗升压药VP阻滞剂后，LE大鼠对AV 3V刺激的反应表现出AP和HR的更大降低和更小的阻力变化。我们的数据表明，心血管反应引起的刺激AV 3V区域可能取决于，在一定程度上，在一个中央加压素机制。
Central vasopressin (VP) may modulate the functional activity of specific neuronal systems involved in cardiovascular regulation. To test this hypothesis we compared cardiovascular (CV) responses to electrical stimulation of the anteroventral region of the third ventricle (AV3V) in Brattleboro rats homozygous for diabetes insipidus (DI), in heterozygous DI rats (DI-HZ) and in normal Long-Evans rats (LE). We also studied the effects of peripheral and intracerebroventricular (ivt) treatment of DI rats with VP and treatment of LE rats with an antipressor blocker of VP on cardiovascular responses to AV3V stimulation. Stimulation of the AV3V region in anesthetized LE rats produced a frequency-dependent increase in renal (RVR) and mesenteric vascular resistance (MVR), a decrease in hindquarter vascular resistance (HQVR), and a decrease in arterial pressure (AP) and heart rate (HR). DI and DI-HZ rats showed significantly greater decreases in AP and HR and lesser changes in RVR, MVR, and HQVR. The deficiency in vasoconstriction in DI rats appeared to be centrally mediated inasmuch as vascular responses to peripherally administered phenylephrine and nerve stimulation were comparable in LE and DI rats. Treatment of DI rats with VP peripherally improved CV responses to AV3V stimulation. An even greater improvement in CV responses to AV3V stimulation was obtained when DI were given ivt infusion of VP. Finally, following intravenous administration of an antipressor VP blocker LE rats showed a greater decrease in AP and HR and lesser resistance changes in response to AV3V stimulation. Our data suggest that cardiovascular responses elicited from stimulation of the AV3V region may depend, in part, on a central vasopressin mechanism.