Morimoto S, Sasaki S, Miki S, Kawa T, Itoh H, Nakata T, Takeda K, Nakagawa M, Naruse S, Maeda T
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Hypertension. 1997 Jan;29(1 Pt 2):514-8. doi: 10.1161/01.hyp.29.1.514.
The rostral ventrolateral medulla (RVLM) has been known to be a major regulating center of sympathetic and cardiovascular activities. An association between essential hypertension and neurovascular compression of the RVLM has been reported in clinical observations, including magnetic resonance imaging (MRI) studies. To reconfirm this relationship, we performed MRI using a high-resolution 512 x 512 matrix in patients with essential and secondary hypertension and in normotensive subjects. The duration of hypertension and the degree of organ damage by hypertension were not significantly different between the two hypertension groups. Neurovascular compression of the RVLM was observed in 74% of the essential hypertension group, and the incidence of compression was significantly higher than in the secondary hypertension group (11%) or in the normotensive group (13%) (P < .01). These results from the clinical studies suggest that neurovascular compression of the RVLM is, at least in part, causally related to essential hypertension. Although blood pressure elevation by pulsatile compression of the RVLM in an experimental baboon model has already been reported, its underlying mechanism is not well known. Accordingly, we performed experiments to investigate whether pulsatile compression of the RVLM would increase arterial pressure and to elucidate the mechanism of the pressor response in rats. Sympathetic nerve activity, arterial pressure, heart rate, and plasma levels of epinephrine and norepinephrine were increased by pulsatile compression of the RVLM. The pressor response was abolished by intravenous treatment with hexamethonium or RVLM injection of kainic acid. In summary, the results from the MRI studies suggest that neurovascular compression of the RVLM is, at least in part, causally related to essential hypertension. This was supported by the results from experimental studies using rats indicating that pulsatile compression of the RVLM increases arterial pressure by enhancing sympathetic outflow.
延髓头端腹外侧区（RVLM）一直被认为是交感神经和心血管活动的主要调节中心。临床观察，包括磁共振成像（MRI）研究，已报道原发性高血压与RVLM的神经血管受压之间存在关联。为了再次证实这种关系，我们对原发性高血压患者、继发性高血压患者和血压正常的受试者使用高分辨率512×512矩阵进行了MRI检查。两组高血压患者的高血压病程和高血压所致器官损害程度无显著差异。原发性高血压组中74%观察到RVLM的神经血管受压，其受压发生率显著高于继发性高血压组（11%）或血压正常组（13%）（P<0.01）。这些临床研究结果表明，RVLM的神经血管受压至少在一定程度上与原发性高血压存在因果关系。尽管已经报道了在实验狒狒模型中通过对RVLM进行搏动性压迫可使血压升高，但其潜在机制尚不清楚。因此，我们进行了实验，以研究对RVLM进行搏动性压迫是否会升高动脉血压，并阐明大鼠升压反应的机制。对RVLM进行搏动性压迫可使交感神经活动、动脉血压、心率以及肾上腺素和去甲肾上腺素的血浆水平升高。静脉注射六甲铵或向RVLM注射 kainic 酸可消除升压反应。总之，MRI研究结果表明，RVLM的神经血管受压至少在一定程度上与原发性高血压存在因果关系。使用大鼠的实验研究结果支持了这一点，表明对RVLM进行搏动性压迫可通过增强交感神经输出而升高动脉血压。
