Parry L J, Summerlee A J
Ontario Veterinary College, University of Guelph, Canada.
Endocrinology. 1991 Jul;129(1):47-52. doi: 10.1210/endo-129-1-47.
Experiments were conducted to investigate the role of the brain angiotensin system in mediating the pressor effects of porcine relaxin in anesthetized female rats. Continuous intracerebroventricular infusion of a specific angiotensin II receptor antagonist (Sar1-Ala8-angiotensin II) completely negated the pressor response to centrally administered relaxin, but only partially suppressed the increase in blood pressure observed after iv injection of the hormone. These results indicate that the pressor effects of relaxin may be mediated, at least in part, by brain angiotensin. Rats with a compromised central angiotensin system were then treated in combination with a peripheral vasopressin (V1) receptor antagonist. Only after both treatments were the pressor effects of iv relaxin completely negated. These data imply that there is also a significant pressor action of relaxin which is independent of the brain angiotensin system. The most likely alternative is a direct action of relaxin on the neural lobe of the pituitary, to provoke the release of vasopressin.
进行实验以研究脑内血管紧张素系统在介导猪松弛素对麻醉雌性大鼠的升压作用中的作用。持续脑室内注入特异性血管紧张素II受体拮抗剂（Sar1-Ala8-血管紧张素II）完全消除了对中枢给予松弛素的升压反应，但仅部分抑制了静脉注射该激素后观察到的血压升高。这些结果表明，松弛素的升压作用可能至少部分由脑内血管紧张素介导。然后将中枢血管紧张素系统受损的大鼠与外周血管加压素（V1）受体拮抗剂联合治疗。仅在两种治疗后，静脉注射松弛素的升压作用才完全消除。这些数据表明，松弛素还存在显著的升压作用，且该作用独立于脑内血管紧张素系统。最可能的替代途径是松弛素对垂体神经叶的直接作用，以促使血管加压素释放。
