Inoue M, Crofton J T, Share L
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.
Exp Brain Res. 1990;83(1):131-6. doi: 10.1007/BF00232201.
Experiments were carried out in conscious, unrestrained, male rats to evaluate possible interactions between brain prostanoids and the brain renin-angiotensin system in the control of vasopressin release and in cardiovascular regulation. The intracerebroventricular (icv) administration of prostaglandin D2 (PGD2) resulted in transient increases in the plasma vasopressin concentration (PAVP) and heart rate and a gradual increase in mean arterial blood pressure (MABP). Pretreatment icv with saralasin, an angiotensin II-receptor antagonist, moderately attenuated the vasopressin response to PGD2, but had no effect on the heart rate and blood pressure responses. Angiotensin II icv increased both PAVP and MABP. This vasopressin response was almost completely prevented by prior icv meclofenamate, a cyclooxygenase inhibitor, and the blood pressure response was attenuated. These observations, combined with previous studies of the role of central angiotensin II and central prostanoids in the physiological control of vasopressin release, suggest that there may be important interactions between brain prostanoids and the brain renin-angiotensin system in this control.
实验在清醒、无拘束的雄性大鼠身上进行，以评估脑内前列腺素和脑肾素 - 血管紧张素系统在控制血管加压素释放及心血管调节方面可能存在的相互作用。脑室内（icv）注射前列腺素D2（PGD2）导致血浆血管加压素浓度（PAVP）和心率短暂升高，平均动脉血压（MABP）逐渐升高。预先脑室内注射血管紧张素II受体拮抗剂沙拉新，可适度减弱血管加压素对PGD2的反应，但对心率和血压反应无影响。脑室内注射血管紧张素II可使PAVP和MABP均升高。预先脑室内注射环氧化酶抑制剂甲氯芬那酸几乎完全阻止了这种血管加压素反应，且血压反应减弱。这些观察结果，结合先前关于中枢血管紧张素II和中枢前列腺素在血管加压素释放生理控制中作用的研究，表明在这种控制中脑内前列腺素和脑肾素 - 血管紧张素系统之间可能存在重要的相互作用。
