Orbai P, Gozariu L, Barabaş E, Strîmbu C, Strîmbu M
Endocrinological Clinic, Institute of Medicine and Pharmacy, Cluj-Napoca, Romania.
Endocrinologie. 1990 Apr-Jun;28(2):47-50.
Magnesemia was determined in male rats weighting 120 +/- 10 g after intravenous administration of nifedipine, an antagonist of calcium channels, and BAY-K 8644, an activator of calcium channels. Nifedipine does not alter the basal level of serum Mg 30 minutes after administration in normal animals or in animals in which chemical sympathectomy was induced by administration of 6 OH-dopamine. On the other hand, BAY-K 8644 induces a significant rise of basal magnesemia from 2.1 +/- 0.2 mg% to 2.7 +/- 0.1 mg% in normal animals. In animals sympathectomized with 6 OH-dopamine, their rise is maintained at about the same level from 2.0 +/- 0.1 mg% after administration). Propranolol previously administered inhibits the stimulating action induced by the calcium channel agonist, BAY-K 8644.
在静脉注射钙通道拮抗剂硝苯地平以及钙通道激活剂BAY-K 8644后，对体重120±10克的雄性大鼠进行血镁测定。在正常动物或经注射6-羟基多巴胺诱导化学交感神经切除的动物中，硝苯地平在给药30分钟后不会改变血清镁的基础水平。另一方面，在正常动物中，BAY-K 8644可使基础血镁水平从2.1±0.2毫克%显著升至2.7±0.1毫克%。在用6-羟基多巴胺进行交感神经切除的动物中，给药后其血镁水平从2.0±0.1毫克%升至大致相同水平并维持。预先给予的普萘洛尔可抑制钙通道激动剂BAY-K 8644诱导的刺激作用。
