Blum J W, Guillebeau A, Binswanger U, Kunz P, Da Prada M, Fischer J A
Acta Endocrinol (Copenh). 1978 Jul;88(3):535-44. doi: 10.1530/acta.0.0880535.
Experiments were designed to investigate responses of immunoreactive parathyroid hormone (PTH) during alpha-adrenergic stimulation and blockade in cows. Alpha-adrenergic agonists (methoxamine, phenylephrine and noradrenaline, the beta-adrenergic action of which was blocked by propranolol) did not change PTH and free fatty acid levels, whereas they characteristically increased the blood pressure and decreased the heart rate. In contrast, alpha-adrenergic blockade by phentolamine progressively increased PTH levels. The elevated PTH concentrations, associated with increased plasma noradrenaline and free fatty acid levels, rising heart rate and decreasing blood pressure, indicated that all these changes can be related to a beta-adrenergic stimulatory mechanism. Beta-adrenergic stimulation was presumably responsible for the initial elevation of PTH concentrations, whereas, during the later phase of the phentolamine infusions, a concomitant hypocalcaemia probably also produced a stimulatory effect.
设计实验以研究奶牛在α-肾上腺素能刺激和阻断过程中免疫反应性甲状旁腺激素（PTH）的反应。α-肾上腺素能激动剂（甲氧明、去氧肾上腺素和去甲肾上腺素，其β-肾上腺素能作用被普萘洛尔阻断）不会改变PTH和游离脂肪酸水平，而它们会典型地升高血压并降低心率。相比之下，酚妥拉明对α-肾上腺素能的阻断会使PTH水平逐渐升高。升高的PTH浓度，与血浆去甲肾上腺素和游离脂肪酸水平升高、心率加快和血压降低相关，表明所有这些变化可能与β-肾上腺素能刺激机制有关。β-肾上腺素能刺激可能是PTH浓度最初升高的原因，而在酚妥拉明输注的后期阶段，伴随的低钙血症可能也产生了刺激作用。
