Sanfield J A, Shenker Y, Grekin R J, Rosen S G
Am J Physiol. 1987 Jun;252(6 Pt 1):E740-5. doi: 10.1152/ajpendo.1987.252.6.E740.
Six normal human subjects each underwent sequential 80-min infusions of saline and epinephrine (EPI) at 0.55 and 2.75 micrograms X min-1 X m-2 to determine the role of EPI in the control of atrial natriuretic hormone (ANH) in humans. Plasma immunoreactive-ANH (IR-ANH) levels nearly doubled in response to the infusion of EPI at 0.55 microgram X min-1 X m-2 (P less than 0.05) and then plateaued; heart rate accelerated significantly (P less than 0.01) with increasing plasma EPI levels, whereas systolic blood pressure increased only with higher plasma EPI levels (P less than 0.05). To determine whether beta-adrenergic mechanisms mediate the EPI-induced increase in IR-ANH, six additional subjects each received infusions on two separate days of saline for 240 min and the beta-adrenergic antagonist propranolol followed by propranolol plus EPI at 2.75 micrograms X min-1 X min-2 each for 80 min. Neither saline nor propranolol plus EPI caused a significant increase in plasma IR-ANH. We conclude that EPI increases plasma IR-ANH through beta-adrenergic mechanisms in humans. beta-Adrenergic-mediated increases in plasma IR-ANH levels appear to be unrelated to changes in the heart rate.
六名正常人类受试者每人依次接受了80分钟的生理盐水和肾上腺素（EPI）输注，输注速率分别为0.55和2.75微克·分钟⁻¹·米⁻²，以确定EPI在人类心房利钠激素（ANH）调控中的作用。输注速率为0.55微克·分钟⁻¹·米⁻²的EPI时，血浆免疫反应性ANH（IR-ANH）水平几乎翻倍（P<0.05），随后趋于平稳；随着血浆EPI水平升高，心率显著加快（P<0.01），而收缩压仅在血浆EPI水平较高时升高（P<0.05）。为了确定β-肾上腺素能机制是否介导了EPI诱导的IR-ANH升高，另外六名受试者在两个不同的日子里分别接受了240分钟的生理盐水输注，之后是β-肾上腺素能拮抗剂普萘洛尔，然后是普萘洛尔加EPI，输注速率均为2.75微克·分钟⁻¹·米⁻²，每次80分钟。生理盐水和普萘洛尔加EPI均未引起血浆IR-ANH显著升高。我们得出结论，在人类中EPI通过β-肾上腺素能机制增加血浆IR-ANH。β-肾上腺素能介导的血浆IR-ANH水平升高似乎与心率变化无关。
