Anderson I K, Ramage A G, Gardiner S M
Department of Physiology and Pharmacology, University of Nottingham Medical School, Queen's Medical Centre, United Kingdom.
Am J Physiol. 1996 Aug;271(2 Pt 2):R455-63. doi: 10.1152/ajpregu.1996.271.2.R455.
The regional hemodynamic changes caused by intracerebroventricular 5-hydroxytryptamine (5-HT) were investigated in conscious Long-Evans and Brattleboro rats with chronically implanted Doppler flow probes. In both strains, a low dose of 5-HT (4 nmol/kg) caused a pressor response associated with tachycardia, mesenteric vasoconstriction, and a transient hindquarters vasodilatation. In Long-Evans rats, higher doses of 5-HT (40 and 120 nmol/kg) caused a pressor response, a bradycardia, mesenteric vasoconstriction, and maintained hindquarters dilatation. The bradycardia and mesenteric vasoconstriction caused by 40 nmol/kg of 5-HT in Long-Evans rats were attenuated by d(CH2)5Tyr(Me)arginine vasopressin, a V1-receptor antagonist. In Brattleboro rats the high doses of 5-HT failed to cause a pressor response but caused a delayed depressor response, a transient tachycardia, less mesenteric vasoconstriction, and a larger initial hindquarters dilatation compared with Long-Evans rats. The initial part of the hindquarters vasodilator response caused by 120 nmol/kg of 5-HT in Brattleboro rats was attenuated by the beta 2-adrenoceptor antagonist ICI-118551. In Long-Evans rats, N,N-di-n-propyl-5-carboxamidotryptamine maleate (DP-5-CT; 3, 30, and 100 nmol/kg icv), a 5-HT1A receptor agonist, caused a tachycardia associated with a marked hindquarters vasodilatation. These changes were accompanied by a weak mesenteric vasoconstriction and, for the highest dose of DP-5-CT, a pressor response. These data overall are consistent with the hemodynamic effects of intracerebroventricular 5-HT contingent on vasopressin release and, along with DP-5-CT, sympathoadrenal excitation; however, additional mechanisms are indicated.
采用长期植入多普勒血流探头的清醒Long-Evans大鼠和Brattleboro大鼠，研究了脑室内注射5-羟色胺（5-HT）引起的局部血流动力学变化。在这两种品系的大鼠中，低剂量的5-HT（4 nmol/kg）引起与心动过速、肠系膜血管收缩和短暂性后肢血管扩张相关的升压反应。在Long-Evans大鼠中，较高剂量的5-HT（40和120 nmol/kg）引起升压反应、心动过缓、肠系膜血管收缩，并维持后肢血管扩张。V1受体拮抗剂d(CH2)5Tyr(Me)精氨酸加压素可减弱Long-Evans大鼠中40 nmol/kg的5-HT引起的心动过缓和肠系膜血管收缩。在Brattleboro大鼠中，高剂量的5-HT未能引起升压反应，但引起延迟的降压反应、短暂性心动过速、肠系膜血管收缩较轻，与Long-Evans大鼠相比，初始后肢血管扩张更大。Brattleboro大鼠中120 nmol/kg的5-HT引起的后肢血管扩张反应的初始部分被β2肾上腺素能受体拮抗剂ICI-118551减弱。在Long-Evans大鼠中，5-HT1A受体激动剂N,N-二正丙基-5-羧酰胺色胺马来酸盐（DP-5-CT；3、30和100 nmol/kg，脑室内注射）引起与明显的后肢血管扩张相关的心动过速。这些变化伴有轻微的肠系膜血管收缩，对于最高剂量的DP-5-CT，还伴有升压反应。总体而言，这些数据与脑室内5-HT的血流动力学效应取决于血管加压素释放以及与DP-5-CT一起引起的交感肾上腺兴奋一致；然而，也表明存在其他机制。
