Takata S, Ogawa J, Oukuwa H, Maeno K, Igarashi A, Terasaki T, Ikeda T, Hattori N
First Department of Internal Medicine, Kanazawa University, Japan.
Clin Exp Hypertens A. 1989;11 Suppl 1:295-301. doi: 10.3109/10641968909045434.
To determine whether cholinergic mechanisms contribute to blood pressure regulation, we examined the effects of atropine on pressor responses to phenylephrine and vasoconstrictor responses to the cold pressor test (CPT) and lower body negative pressure (LBNP) in 16 healthy subjects. Heart rate, blood pressure and cardiac index were significantly increased, and central venous pressure (CVP) was significantly decreased after atropine (0.04mg/kg). After atropine, pressor responses to phenylephrine at doses of 20, 40 and 80 micrograms were significantly increased by 101, 112 and 93% (p less than 0.001); however, atropine attenuated pressor responses to CPT (p less than 0.001) and forearm vasoconstrictor responses to LBNP. In 6 propranolol-treated subjects, atropine also augmented pressor responses to phenylephrine but attenuated pressor responses to CPT. These results suggest that atropine augments the pressor response to an alpha-agonist, which may be partly explained by inhibition of compensatory vascular responses mediated by cholinergic mechanisms.
为了确定胆碱能机制是否有助于血压调节，我们在16名健康受试者中研究了阿托品对去氧肾上腺素升压反应以及冷加压试验（CPT）和下体负压（LBNP）引起的血管收缩反应的影响。给予阿托品（0.04mg/kg）后，心率、血压和心脏指数显著升高，中心静脉压（CVP）显著降低。给予阿托品后，20、40和80微克剂量的去氧肾上腺素升压反应分别显著增加101%、112%和93%（p<0.001）；然而，阿托品减弱了对CPT的升压反应（p<0.001）以及对LBNP的前臂血管收缩反应。在6名接受普萘洛尔治疗的受试者中，阿托品也增强了对去氧肾上腺素的升压反应，但减弱了对CPT的升压反应。这些结果表明，阿托品增强了对α激动剂的升压反应，这可能部分是由于抑制了胆碱能机制介导的代偿性血管反应。
