Unger T, Rohmeiss P, Demmert G, Luft F C, Ganten D, Lang R E
J Cardiovasc Pharmacol. 1986;8 Suppl 7:S81-6. doi: 10.1097/00005344-198600087-00016.
The central cardiovascular actions of arginine vasopressin (AVP) and the role of this peptide in the modulation of baroreceptor reflex (BRR) sensitivity were investigated in conscious, chronically instrumented rats. Intracerebroventricular (i.c.v.) injections of AVP (1-100 ng) produced dose-dependent pressor effects together with increases in heart rate, splanchnic, and renal sympathetic nerve activity and a reduction of mesenteric blood flow. These responses were prevented by i.c.v. pretreatment with a V1-AVP receptor antagonist. Furthermore, the central pressor effects of AVP were abolished by peripheral alpha-adrenoceptor blockade with phentolamine. In contrast to the i.c.v. injections, intravenous (i.v.) or intracarotid injections of AVP produced pressor responses accompanied by bradycardia and a decrease in sympathetic nerve activity. Intracerebroventricular pretreatment with a V1-AVP receptor antagonist shifted the slope of the BRR curve (increases in pulse interval plotted against increases in systolic blood pressure in response to i.v. methoxamine) toward higher sensitivity, whereas i.v. pretreatment with a V2-AVP receptor antagonist shifted the slope of the BRR curve toward lower sensitivity of the reflex. These findings suggest that central (neuronal) AVP, by acting on V1-AVP receptors in the brain, participates in central pressor mechanisms, activates the sympathetic nervous system, and desensitizes the BRR. Conversely, circulating (hormonal) AVP can sensitize the BRR by acting on V2-AVP receptors accessible from the blood. Our data provide evidence pointing to a direct interaction between the neuronal and the hormonal axis of the AVP system within cardiovascular control.
在清醒、长期植入仪器的大鼠中，研究了精氨酸加压素（AVP）的中枢心血管作用及其在压力感受器反射（BRR）敏感性调节中的作用。脑室内（i.c.v.）注射AVP（1 - 100 ng）产生剂量依赖性的升压作用，同时心率、内脏和肾交感神经活动增加，肠系膜血流量减少。这些反应可被i.c.v.预先使用V1 - AVP受体拮抗剂所阻断。此外，酚妥拉明对外周α - 肾上腺素能受体的阻断可消除AVP的中枢升压作用。与i.c.v.注射不同，静脉内（i.v.）或颈内注射AVP产生升压反应并伴有心动过缓和交感神经活动减少。用V1 - AVP受体拮抗剂进行脑室内预处理可使BRR曲线的斜率（静脉注射甲氧明时，脉搏间期增加与收缩压增加的关系）向更高敏感性偏移，而用V2 - AVP受体拮抗剂进行静脉内预处理可使BRR曲线的斜率向反射的更低敏感性偏移。这些发现表明，中枢（神经元）AVP通过作用于脑中的V1 - AVP受体，参与中枢升压机制，激活交感神经系统，并使BRR脱敏。相反，循环（激素）AVP可通过作用于血液中可及的V2 - AVP受体使BRR敏感化。我们的数据提供了证据，表明AVP系统的神经元轴和激素轴在心血管控制中存在直接相互作用。
