Rankin A J, Courneya C A, Wilson N, Ledsome J R
Life Sci. 1986 May 26;38(21):1951-7. doi: 10.1016/0024-3205(86)90224-9.
In anesthetized, vagotomized rabbits the plasma concentration of immunoreactive atrial natriuretic peptide (IR-ANP) was found to be 58.5 +/- 3.4 pg/mL (n = 18) when measured using a radio-immunoassay. Tachycardia, induced by electrical pacing of the right atrium, resulted in increased plasma levels of IR-ANP. The size of the increase in IR-ANP appeared to be related to the degree of tachycardia induced. The release of IR-ANP with tachycardia was unaffected by beta-adrenergic blockade with atenolol (2 mg/kg), muscarinic blockade with atropine (2 mg/kg) or ganglionic blockade with hexamethonium (10 mg/kg). The results show that IR-ANP is released in response to tachycardia and that this does not involve a neuronal reflex.
在麻醉、迷走神经切断的兔中，使用放射免疫分析法测量时，发现免疫反应性心房利钠肽（IR-ANP）的血浆浓度为58.5±3.4 pg/mL（n = 18）。右心房电起搏诱导的心动过速导致IR-ANP血浆水平升高。IR-ANP升高的幅度似乎与诱导的心动过速程度有关。心动过速时IR-ANP的释放不受阿替洛尔（2 mg/kg）的β-肾上腺素能阻滞、阿托品（2 mg/kg）的毒蕈碱阻滞或六甲铵（10 mg/kg）的神经节阻滞影响。结果表明，IR-ANP是对心动过速作出反应而释放的，且这一过程不涉及神经反射。
