Dahlöf P, Lundberg J M, Dahlöf C
Department of Clinical Pharmacology, Sahlgrenska Hospital, Gothenburg University, Sweden.
Neuropeptides. 1991 Apr;18(4):171-80. doi: 10.1016/0143-4179(91)90144-8.
The effect of exogenous angiotensin II (A II) and the angiotensin converting enzyme (ACE)-inhibitor captopril on plasma levels of neuropeptide Y-like immunoreactivity (NPY-LI) has been studied in the pithed guinea pig. Four periods of pre-ganglionic nerve stimulation (PNS, 8 Hz for 30s with 20 min intervals) were applied and the increases of mean arterial blood pressure (delta BP), heart rate (delta HR) and plasma NPY-LI (delta NPY-LI) in response to PNS were analysed in non-pre-treated and captopril pre-treated animals. Captopril (5 mg x kg-1 i.v.) reduced basal blood pressure and delta BP by 20% and 11%, respectively. Infusion of A II (0.5 microgram x kg-1 = min-1 i.v.) caused a significant increase in basal and PNS-induced maximal blood pressure response but reduced delta BP in captopril and non-pre-treated animals by 40% and 16%, respectively. A II elicited a long-lasting increase of basal heart rate by 12% but reduced delta HR by 36% in non-pre-treated animals. However, neither captopril alone nor A II infusion to captopril pre-treated animals significantly changed heart-rate values. The effects of exogenous A II on the cardiovascular responses were abolished by the A II-antagonist saralasin (a bolus injection, 40 micrograms x kg-1 i.v. followed by an infusion, 30 micrograms x kg-1 x min-1), which per se had no significant effect. Captopril pre-treatment reduced basal plasma NPY-LI levels by 38% and delta NPY-LI by 46% in response to PNS 1. However, neither in non-pre-treated nor in captopril pre-treated animals did infusion of A II significantly change the plasma NPY-LI level.(ABSTRACT TRUNCATED AT 250 WORDS)
在麻醉的豚鼠身上研究了外源性血管紧张素II（A II）和血管紧张素转换酶（ACE）抑制剂卡托普利对血浆神经肽Y样免疫反应性（NPY-LI）水平的影响。施加四个节前神经刺激期（PNS，8Hz，持续30秒，间隔20分钟），并分析未预处理和卡托普利预处理动物对PNS的平均动脉血压升高（δBP）、心率升高（δHR）和血浆NPY-LI升高（δNPY-LI）情况。卡托普利（5mg·kg-1静脉注射）分别使基础血压和δBP降低20%和11%。输注A II（0.5μg·kg-1·min-1静脉注射）导致基础血压和PNS诱导的最大血压反应显著升高，但在卡托普利处理组和未处理组动物中分别使δBP降低40%和16%。A II使基础心率长期升高12%，但在未处理动物中使δHR降低36%。然而，单独使用卡托普利或对卡托普利预处理动物输注A II均未显著改变心率值。A II拮抗剂沙拉新（静脉推注40μg·kg-1，随后输注30μg·kg-1·min-1）消除了外源性A II对心血管反应的影响，而沙拉新本身无显著作用。卡托普利预处理使基础血浆NPY-LI水平降低38%，对PNS 1的反应使δNPY-LI降低46%。然而，在未处理组和卡托普利预处理组动物中，输注A II均未显著改变血浆NPY-LI水平。（摘要截断于250字）
