Currie M G, Newman W H
Biochem Biophys Res Commun. 1986 May 29;137(1):94-100. doi: 10.1016/0006-291x(86)91180-0.
Atrial myocardium is the source of a recently described peptide hormone termed atriopeptin. Atriopeptin is thought to have a role in the regulation of systemic arterial pressure, fluid balance and plasma electrolyte homeostasis. Isolated rat hearts release atriopeptin into the coronary effluent, and we have found that this release is stimulated by the administration of norepinephrine, a compound with alpha and beta adrenergic properties. Infusion of the pure beta-receptor agonist, isoproterenol, failed to stimulate the release; however, the alpha-1 receptor agonist phenylephrine induced the release in a dose-dependent manner. The stimulation of atriopeptin release by norepinephrine and phenylephrine was inhibited by alpha-blockade with phentolamine. Administration of BHT-920, a selective alpha-2 agonist, had no effect on atriopeptin release. We conclude that atriopeptin secretion by the atrial myocyte is stimulated by activation of the alpha-1 adrenergic receptor. This finding suggests an involvement of the sympathetic nervous system in the physiologic regulation of the secretion of this hormone.
心房肌是一种最近被描述的称为心房肽的肽类激素的来源。心房肽被认为在全身动脉压、体液平衡和血浆电解质稳态的调节中起作用。离体大鼠心脏将心房肽释放到冠状流出液中,并且我们发现这种释放受到去甲肾上腺素(一种具有α和β肾上腺素能特性的化合物)的给药刺激。输注纯β受体激动剂异丙肾上腺素未能刺激释放;然而,α-1受体激动剂去氧肾上腺素以剂量依赖的方式诱导释放。去甲肾上腺素和去氧肾上腺素对心房肽释放的刺激被酚妥拉明的α阻断所抑制。给予选择性α-2激动剂BHT-920对心房肽释放没有影响。我们得出结论,心房肌细胞分泌心房肽是由α-1肾上腺素能受体的激活所刺激的。这一发现表明交感神经系统参与了这种激素分泌的生理调节。