Corder R, Lowry P J, Wilkinson S J, Ramage A G
Eur J Pharmacol. 1986 Feb 11;121(1):25-30. doi: 10.1016/0014-2999(86)90388-2.
Blood pressure, heart rate, cardiac output, renal flow and femoral flow were recorded in open-chested anaesthetised cats. Dose-response curves were constructed for neuropeptide Y, angiotensin II and noradrenaline after pretreatment with atropine sulphate. Neuropeptide Y, on a molar basis, was 7 and 120 times less potent than noradrenaline and angiotensin, respectively, in producing a 50 mm Hg rise in mean arterial blood pressure. The pressor effect of neuropeptide Y was characterised by dose-dependent increases in total peripheral, renal and femoral resistance with little change in cardiac output. Neuropeptide Y had a similar potency to noradrenaline in causing these resistance changes. However, the pressor response to noradrenaline was associated with a dose-dependent increase in cardiac output. The pressor action of neuropeptide Y was not attenuated by adrenoceptor blockade by phenoxybenzamine (5 mg kg-1) and propranolol (1 mg kg-1).
在开胸麻醉的猫身上记录血压、心率、心输出量、肾血流量和股血流量。在用硫酸阿托品预处理后,构建了神经肽Y、血管紧张素II和去甲肾上腺素的剂量反应曲线。以摩尔为基础,神经肽Y在使平均动脉血压升高50 mmHg时,其效力分别比去甲肾上腺素和血管紧张素低7倍和120倍。神经肽Y的升压作用表现为总外周阻力、肾阻力和股阻力随剂量依赖性增加,而心输出量变化不大。神经肽Y在引起这些阻力变化方面与去甲肾上腺素具有相似的效力。然而,去甲肾上腺素的升压反应与心输出量随剂量依赖性增加有关。神经肽Y的升压作用不会被酚苄明(5 mg kg-1)和普萘洛尔(1 mg kg-1)的肾上腺素能受体阻断所减弱。