Kumagai H, Suzuki H, Ryuzaki M, Matsukawa S, Saruta T
Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.
Circ Res. 1990 Dec;67(6):1309-22. doi: 10.1161/01.res.67.6.1309.
Conscious normotensive and two-kidney, one-clip Goldblatt hypertensive rabbits were studied to determine the sensitivity of the arterial baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate. The relations of the mean arterial pressure-RSNA and mean arterial pressure-heart rate were examined over a wide range of blood pressures produced by infusions of phenylephrine and nitroglycerin. The maximum slope obtained by logistic function analysis was considered to represent the baroreflex sensitivity. In the early hypertensive group (n = 8; mean arterial pressure +/- SEM, 88 +/- 2 mm Hg) on day 5 after renal clip application, the maximum slope of the mean arterial pressure-RSNA relation was -11.3 +/- 1.2, which was significantly greater than that of the sham normotensive group (-6.9 +/- 0.3, p less than 0.05). The maximum slope (-4.3 +/- 0.2) of the mean arterial pressure-RSNA relation in the late hypertensive group (n = 8; mean arterial pressure, 96 +/- 3 mm Hg) on day 21 after renal clipping was significantly smaller than that of another sham group (-7.2 +/- 0.2, p less than 0.05). In contrast to these changes in the baroreflex control of RSNA, the control of heart rate was attenuated according to the magnitude of mean arterial pressure. To elucidate the mechanisms underlying the potentiated baroreflex, the effects of endogenous neuropeptides were investigated. First, plasma concentrations of angiotensin II and arginine vasopressin that are known to affect the baroreflex were determined. Plasma concentrations of vasopressin (3.1 +/- 0.6 pg/ml) as well as of angiotensin II (34 +/- 7 pg/ml) were increased in the early hypertensive group, and the plasma vasopressin returned to a similar level to the sham group in the late hypertensive group (1.3 +/- 0.4 pg/ml). Second, to study endogenous effects of these neuropeptides on the baroreflex, the maximum slopes of the baroreflex curves during infusions of antagonists for the peptides were determined in the early hypertensive group. The maximum slope of mean arterial pressure-RSNA during intravertebral arterial [Sar1, Ala8]-angiotensin II (-16.4 +/- 1.5) was significantly greater (p less than 0.05), whereas the maximum slope during intravertebral arterial infusion of d(CH2)5Tyr(Me)arginine vasopressin (-4.7 +/- 0.5) was significantly smaller (p less than 0.05) than that during vehicle infusion (-11.3 +/- 1.2).(ABSTRACT TRUNCATED AT 400 WORDS)
对清醒的血压正常和双肾单夹型Goldblatt高血压兔进行研究，以确定肾交感神经活动（RSNA）和心率的动脉压力感受器反射控制的敏感性。通过输注去氧肾上腺素和硝酸甘油产生广泛的血压范围，检测平均动脉压-RSNA和平均动脉压-心率之间的关系。通过逻辑函数分析获得的最大斜率被认为代表压力感受器反射敏感性。在肾夹闭术后第5天的早期高血压组（n = 8；平均动脉压±标准误，88±2 mmHg）中，平均动脉压-RSNA关系的最大斜率为-11.3±1.2，显著大于假手术血压正常组（-6.9±0.3，p<0.05）。肾夹闭术后第21天的晚期高血压组（n = 8；平均动脉压，96±3 mmHg）中，平均动脉压-RSNA关系的最大斜率（-4.3±0.2）显著小于另一假手术组（-7.2±0.2，p<0.05）。与RSNA的压力感受器反射控制的这些变化相反，心率的控制根据平均动脉压的幅度而减弱。为了阐明压力感受器反射增强的潜在机制，研究了内源性神经肽的作用。首先，测定已知影响压力感受器反射的血管紧张素II和精氨酸加压素的血浆浓度。早期高血压组中加压素（3.1±0.6 pg/ml）以及血管紧张素II（34±7 pg/ml）的血浆浓度升高，晚期高血压组中血浆加压素恢复到与假手术组相似的水平（1.3±0.4 pg/ml）。其次，为了研究这些神经肽对压力感受器反射的内源性作用，在早期高血压组中测定肽拮抗剂输注期间压力感受器反射曲线的最大斜率。椎动脉内注射[Sar1，Ala8]-血管紧张素II期间平均动脉压-RSNA的最大斜率（-16.4±1.5）显著更大（p<0.05），而椎动脉内注射d(CH2)5Tyr(Me)精氨酸加压素期间的最大斜率（-4.7±0.5）显著小于注射溶媒期间的最大斜率（-11.3±1.2，p<0.05）。（摘要截短至400字）
