Takemoto Y
Department of Physiology, Hiroshima University School of Medicine, Minami-ku, Japan.
Jpn J Physiol. 1995;45(5):743-58. doi: 10.2170/jjphysiol.45.743.
Electromagnetic flow probes were used to measure regional blood flow responses to central injection of L-proline in conscious rats. Ten min after intracisternal injection of 10 mumol of L-proline, arterial pressure increased from 113 +/- 1.6 (mean +/- SEM, n = 23) to 142 +/- 2.9 mmHg, while the heart rate decreased from 383 +/- 9.6 (n = 23) to 313 +/- 5.4 beats/min, vascular resistance increased an average of 239% in the superior mesenteric artery (n = 8) and 72% in the renal artery (n = 8), without change in the terminal aorta (-6%, n = 7). However, 10 mumol of D-proline induced neither blood pressure increase nor bradycardia 10 min after its injection. After sino-aortic denervation, the heart rate was not decreased by L-proline injection. Ganglionic blockade with chlorisondamine evoked significantly greater pressor action by L-proline injection than that without treatment, but intravenous injection of the vasopressin antagonist, (d(CH2)5(1), O-Me-Tyr2, Arg8)-vasopressin (10 micrograms/kg), promptly dilated the superior mesenteric vascular bed and lowered the arterial pressure. In addition, pretreatment with the vasopressin antagonist alone almost abolished the pressor and vasoconstrictor action induced by L-proline injection. These results indicate that intracisternal injection of L-proline specifically elicited an increase in arterial pressure mainly through marked vasoconstriction of the superior mesenteric artery bed, and that bradycardia was elicited via the baroreflex. Thus, vasopressin release in the blood-stream was involved in these hemodynamic actions.
使用电磁血流探头测量清醒大鼠脑室内注射L-脯氨酸后局部血流反应。脑室内注射10 μmol L-脯氨酸10分钟后,动脉血压从113±1.6(平均值±标准误,n = 23)升至142±2.9 mmHg,而心率从383±9.6(n = 23)降至313±5.4次/分钟,肠系膜上动脉血管阻力平均增加239%(n = 8),肾动脉血管阻力增加72%(n = 8),终末主动脉无变化(-6%,n = 7)。然而,注射10 μmol D-脯氨酸10分钟后既未引起血压升高也未引起心动过缓。去窦弓神经后,注射L-脯氨酸未使心率降低。用氯异吲哚铵进行神经节阻断后,注射L-脯氨酸引起的升压作用比未治疗时显著增强,但静脉注射血管加压素拮抗剂(d(CH2)5(1), O-Me-Tyr2, Arg8)-血管加压素(10 μg/kg)可迅速扩张肠系膜上血管床并降低动脉血压。此外,单独用血管加压素拮抗剂预处理几乎完全消除了注射L-脯氨酸引起的升压和血管收缩作用。这些结果表明,脑室内注射L-脯氨酸主要通过显著收缩肠系膜上动脉床特异性地引起动脉血压升高,心动过缓是通过压力反射引起的。因此,血流中血管加压素的释放参与了这些血流动力学作用。