Wesslau C
Acta Med Scand Suppl. 1983;672:17-20. doi: 10.1111/j.0954-6820.1983.tb01608.x.
Most beta-adrenergic effects are mediated by activation of the enzyme adenylate cyclase. Hormone binds to the receptor leading to an accelarated binding of GTP to the coupling protein, the N-protein, which is activated. This causes an activation of the adenylate cyclase and an increased formation of cAMP, the intracellular second messenger. The same principles hold good for other hormones coupled to adenylate cyclase. The sensitivity of the adenylate cyclase may be altered in different clinical and experimental conditions. An increased sensitivity is seen in hyperthyroidism in man and in the rat, and during starvation in rats. A decreased sensitivity is seen in hypothyroidism, in patients with pheochromocytoma, pseudohypoparathyroidism type I or multiple symmetric lipomatosis. Several reasons for the altered sensitivity have been suggested. The number of hormone receptors, the coupling between receptor and N-protein, the amount or function of the N-protein or the PDE activity may all vary in different conditions.
大多数β-肾上腺素能效应是由腺苷酸环化酶的激活介导的。激素与受体结合，导致GTP加速与偶联蛋白N蛋白结合，N蛋白被激活。这会引起腺苷酸环化酶的激活以及细胞内第二信使环磷酸腺苷（cAMP）生成增加。同样的原理也适用于与腺苷酸环化酶偶联的其他激素。腺苷酸环化酶的敏感性在不同的临床和实验条件下可能会发生改变。在人类和大鼠的甲状腺功能亢进症以及大鼠饥饿期间，可见敏感性增加。在甲状腺功能减退症、嗜铬细胞瘤患者、I型假性甲状旁腺功能减退症或多发性对称性脂肪瘤病患者中，可见敏感性降低。已经提出了敏感性改变的几个原因。激素受体的数量、受体与N蛋白之间的偶联、N蛋白的量或功能或磷酸二酯酶（PDE）活性在不同条件下可能都会有所不同。
