Tamborini G
Istituto di Cardiologia, Università degli Studi di Milano.
Ann Ital Med Int. 1990 Oct-Dec;5(4 Pt 2):451-8.
The aim of this study was to verify the possible role of serotonin on vascular basal tone and over-reactivity in systemic and pulmonary circuits in hypertensive patients. We studied 15 hypertensive (G1) and 10 normotensive (G2) subjects. Right-side pressure and intravascular-arterial pressure measurements were obtained in baseline conditions and during alpha-adrenergic activation by cold-pressor-test (CPT), before and after intravenous injection of ketanserin 10 mg (K), an S2-receptor antagonist. Systemic and pulmonary pressures and resistances were higher in G1 than in G2 in the steady state. K induced a significant reduction of both pressures and resistances in G1, no change in systemic response to CPT in the 2 groups and a significant reduction in the pulmonary vascular reactivity to adrenergic stimulus only in G1. These data confirm the vasodilator action of serotonin-blockade. The observation of vasodilatation in pulmonary circulation is not in favor of its dependence on vascular endothelium damage. In fact the arterial endothelium lesions due to hypertension are present only in the systemic circuit. Concerning result of CPT: 1) serotonin doesn't seem responsible for vascular over-reactivity in hypertension, unchanged by K; 2) the particular pattern of pulmonary vascular contractility in G1 may be interpreted as resulting from an elective depressive action of S2-blockade, depending on a different distribution of S1 and S2 receptors in the two circuits.
本研究的目的是验证血清素在高血压患者体循环和肺循环中对血管基础张力和过度反应性的可能作用。我们研究了15名高血压患者（G1组）和10名血压正常者（G2组）。在基线条件下以及静脉注射10 mg酮色林（K）（一种S2受体拮抗剂）前后，通过冷加压试验（CPT）进行α-肾上腺素能激活期间，测量右侧压力和血管内动脉压力。在稳态下，G1组的体循环和肺循环压力及阻力均高于G2组。K使G1组的压力和阻力均显著降低，两组对CPT的全身反应均无变化，且仅G1组对肾上腺素能刺激的肺血管反应性显著降低。这些数据证实了血清素阻断的血管舒张作用。肺循环中血管舒张的观察结果不支持其依赖于血管内皮损伤。事实上，高血压引起的动脉内皮病变仅存在于体循环中。关于CPT的结果：1）血清素似乎与高血压中的血管过度反应性无关，K对其无影响；2）G1组中肺血管收缩的特殊模式可解释为是由于S2阻断的选择性抑制作用，这取决于两个循环中S1和S2受体的不同分布。
