VASCULAR TONE INFLUENCES ARTERIAL-PRESSURE LABILITY AFTER SINOAORTIC DEAFFERENTATION
VASCULAR TONE INFLUENCES ARTERIAL-PRESSURE LABILITY AFTER SINOAORTIC DEAFFERENTATION
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DOI：
10.1152/ajpregu.1991.260.2.r359
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发表时间：
1991-02-01
影响因子：
--
通讯作者：
BRODY, MJ
中科院分区：
文献类型：
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作者：
JACOB, HJ;ALPER, RH;BRODY, MJ
窦主动脉传入阻滞（SAD）导致动脉压变异性增加。 本研究的目的是探讨非神经源性的外周血管扩张机制对动脉压不稳定的影响。 在SAD大鼠中，神经节阻滞联合卡托普利或V1-加压素受体拮抗剂可降低高不稳定性。 在这些条件下，持续输注苯肾上腺素和内源性血管收缩剂血管紧张素II，肾上腺素和加压素增加不稳定性，这表明血管张力的水平是重要的维持不稳定性。 单个血管床的血流动力学变化与压力不稳定性无关;然而，阻力变化的总和（总外周阻力变化的估计值）显著相关。 这些结果表明：1）内源性血管收缩剂的直接作用可能通过维持高背景血管张力而引起动脉压的显著变化; 2）单个血管床阻力的变化不能解释血管收缩剂输注引起的动脉压不稳定性。 我们的结论是，神经和/或体液来源的血管紧张度与压力感受器的传入神经阻滞相关的动脉压波动的产生是至关重要的。
Sinoaortic deafferentation (SAD) results in increased variability of arterial pressure. The purpose of this study was to investigate the contribution of nonneurogenic, peripheral vasomotor mechanisms to this arterial pressure lability. In rats with SAD, ganglionic blockade combined with either captopril or a V1-vasopressin receptor antagonist reduced the high lability. Under these conditions, continuous infusions of phenylephrine and the endogenous vasoconstrictors angiotensin II, epinephrine, and vasopressin increased lability, suggesting that the level of vascular tone is important for maintaining lability. Hemodynamic changes in individual vascular beds did not correlate with pressure lability; however, the sum of the changes in resistance, an estimate of changes in total peripheral resistance, was significantly correlated. These results suggest that 1) direct actions of endogenous vasoconstrictors can induce marked variations of arterial pressure, presumably by sustaining a high background of vascular tone, and 2) variations in resistance of individual vascular beds do not account for the lability of arterial pressure evoked by infusion of vasoconstrictors. We conclude that vascular tone of neural and/or humoral origin is critical for the generation of fluctuations in arterial pressure associated with deafferentation of baroreceptors.