Bernier N J, Kaiya H, Takei Y, Perry S F
Department of Biology, University of Ottawa, 30 Marie Curie, Ottawa, Ontario, Canada K1N 6N5.
J Endocrinol. 1999 Mar;160(3):351-63. doi: 10.1677/joe.0.1600351.
The individual contributions of, and potential interactions between, the renin-angiotensin system (RAS) and the humoral adrenergic stress response to blood pressure regulation were examined in rainbow trout. Intravenous injection of the smooth muscle relaxant, papaverine (10 mg/kg), elicited a transient decrease in dorsal aortic blood pressure (PDA) and systemic vascular resistance (RS), and significant increases in plasma angiotensin II (Ang II) and catecholamine concentrations. Blockade of alpha-adrenoceptors before papaverine treatment prevented PDA and RS recovery, had no effect on the increase in plasma catecholamines, and resulted in greater plasma Ang II concentrations. Administration of the angiotensin-converting enzyme inhibitor, lisinopril (10(-4) mol/kg), before papaverine treatment attenuated the increases in the plasma concentrations of Ang II, adrenaline, and noradrenaline by 90, 79, and 40%, respectively and also prevented PDA and RS recovery. By itself, lisinopril treatment caused a gradual and sustained decrease in PDA and RS, and reductions in basal plasma Ang II and adrenaline concentrations. Bolus injection of a catecholamine cocktail (4 nmol/kg noradrenaline plus 40 nmol/kg adrenaline) in the lisinopril+papaverine-treated trout, to supplement their circulating catecholamine concentrations and mimic those observed in fish treated only with papaverine, resulted in a temporary recovery in PDA and RS. These results indicate that the RAS and the acute humoral adrenergic response are both recruited during an acute hypotensive stress, and have important roles in the compensatory response to hypotension in rainbow trout. However, whereas the contribution of the RAS to PDA recovery is largely indirect and relies on an Ang II-mediated secretion of catecholamines, the contribution from the adrenergic system is direct and relies at least in part on plasma catecholamines.
在虹鳟鱼中研究了肾素 - 血管紧张素系统（RAS）和体液性肾上腺素应激反应对血压调节的个体贡献以及它们之间的潜在相互作用。静脉注射平滑肌松弛剂罂粟碱（10 mg/kg）引起背主动脉血压（PDA）和全身血管阻力（RS）短暂下降，以及血浆血管紧张素II（Ang II）和儿茶酚胺浓度显著升高。在罂粟碱处理前阻断α - 肾上腺素能受体可防止PDA和RS恢复，对血浆儿茶酚胺升高无影响，并导致血浆Ang II浓度升高。在罂粟碱处理前给予血管紧张素转换酶抑制剂赖诺普利（10^(-4) mol/kg）可使Ang II、肾上腺素和去甲肾上腺素的血浆浓度升高分别降低90%、79%和40%，并防止PDA和RS恢复。单独使用赖诺普利治疗会导致PDA和RS逐渐持续下降，以及基础血浆Ang II和肾上腺素浓度降低。在接受赖诺普利 + 罂粟碱治疗的鳟鱼中推注儿茶酚胺混合物（4 nmol/kg去甲肾上腺素加40 nmol/kg肾上腺素），以补充其循环儿茶酚胺浓度并模拟仅用罂粟碱治疗的鱼中观察到的情况，导致PDA和RS暂时恢复。这些结果表明，在急性低血压应激期间，RAS和急性体液性肾上腺素反应均被激活，并且在虹鳟鱼对低血压的代偿反应中起重要作用。然而，RAS对PDA恢复的贡献在很大程度上是间接的，依赖于Ang II介导的儿茶酚胺分泌，而肾上腺素能系统的贡献是直接的，至少部分依赖于血浆儿茶酚胺。
