Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph, Guelph, Ontario N1G 2W1, Canada.
J Neuroendocrinol. 1990 Feb 1;2(1):53-8. doi: 10.1111/j.1365-2826.1990.tb00392.x.
Abstract Experiments were done to examine the pressor effect of iv porcine relaxin in anaesthetized rats. Acute injections of relaxin caused consistent and sustained rises in systemic blood pressure that were dose-dependent within the physiological range. Pretreatment of rats with a specific vasopressin (V1) receptor antagonist, but not an alpha-adrenoreceptor antagonist, substantially reduced the pressor effect of relaxin. After the vasopressin receptor antagonist, small rises in blood pressure occurred after a longer latent period, compared with the responses in intact animals. The data clearly indicate that acute injections of relaxin cause a pressor response that is predominantly affected via the release of vasopressin. The possible sources of the persistent hypertensive component are discussed and it is suggested that relaxin might act through the central angiotensinergic systems to release vasopressin and cause a pressor response.
摘要 本实验旨在研究静脉内给予猪松弛素对麻醉大鼠的升压作用。松弛素急性注射可引起一致且持续的全身血压升高，且在生理范围内呈剂量依赖性。预先给予大鼠特定的血管加压素 (V1) 受体拮抗剂而非 α-肾上腺素受体拮抗剂可显著降低松弛素的升压作用。血管加压素受体拮抗剂预处理后，与完整动物的反应相比，血压升高的潜伏期更长，幅度更小。这些数据清楚地表明，急性给予松弛素会引起主要通过血管加压素释放引起的升压反应。讨论了持续性高血压成分的可能来源，并提出松弛素可能通过中枢血管紧张素能系统作用于血管加压素释放并引起升压反应。
