Lappe R W, Slivjak M J, Todt J A, Wendt R L
Wyeth Laboratories, Inc., Philadelphia, PA 19101.
Regul Pept. 1987 Dec;19(5-6):307-12. doi: 10.1016/0167-0115(87)90172-8.
The cardiovascular effects of calcitonin gene-related peptide (CGRP) were examined in conscious, unrestrained rats. Changes in mean arterial pressure, heart rate and cardiac output were continuously monitored before and after i.v. bolus injection of CGRP (0.1-5 micrograms/kg). Injection of the peptide caused dose-dependent reductions in mean arterial pressure (-24 +/- 4 mmHg), which were accompanied by marked tachycardia. Cardiac output was significantly increased after CGRP but little change was observed in stroke volume. CGRP also reduced total peripheral resistance (-46 +/- 6%). These data indicate that the hypotensive actions of CGRP are mediated through peripheral vasodilation rather than through reductions in cardiac output. Pretreatment with propranolol significantly reduced the tachycardia responses to CGRP from 81 +/- 11 beats/min to 36 +/- 4 beats/min, but did not abolish the increase in heart rate. These data suggest that CGRP produces a tachycardia through reflex increases in cardiac sympathetic tone and through possible direct positive chronotropic effects on the heart.
在清醒、未受束缚的大鼠中研究了降钙素基因相关肽(CGRP)对心血管系统的影响。在静脉推注CGRP(0.1 - 5微克/千克)前后,持续监测平均动脉压、心率和心输出量的变化。注射该肽导致平均动脉压呈剂量依赖性降低(-24±4 mmHg),同时伴有明显的心动过速。CGRP注射后心输出量显著增加,但每搏输出量变化不大。CGRP还降低了总外周阻力(-46±6%)。这些数据表明,CGRP的降压作用是通过外周血管舒张介导的,而非通过降低心输出量。用普萘洛尔预处理可显著降低对CGRP的心动过速反应,从81±11次/分钟降至36±4次/分钟,但并未消除心率的增加。这些数据表明,CGRP通过心脏交感神经张力的反射性增加以及可能对心脏的直接正性变时作用产生心动过速。