Fundamental Research on the Pharmacological Activity of Oriental Drugs. XII. Pharmacological Research on β-Adrenergic Potentiation Factors included in Musk and Their Organ-Selective Activity

Open Access
Publisher Website
Google Scholar
Abstract
Potentiation of .beta.-adrenergic responses by musk, an animal-origin drug, was studied mainly in cat papillary muscle preparations driven by electric stimulation (10 V, 0.8 ms, 0.4 Hz). To isolate the .beta.-adrenergic potentiation factors, musk (20 g) was extracted and the potentiation activity of each fraction was assayed using the cardiac muscle. The resultant fraction W (64 mg) was homogeneous as judged by TLC. Dialyzed W was soluble in ethanol and water but not in ether. The .beta.-adrenergic potentiation of the cardiac muscle induced by W was not due to the inhibition of catechol-O-methyl transferase (COMT) from the following facts: parallelism between the COMT-inhibition activity and the .beta.-adrenergic potentiation activity was not observed among the lots of musk tested, a purified musk fraction was a weaker inhibitor of COMT activity than the crude, and musk induced a potentiation of isoproterenol (IsP) to the same extent even in the high doses by which the inhibitory effect of pronethalol was surmounted. The purified fraction did not potentiate IsP-induced relaxation of smooth muscle preparations of trachea and taenia coli in guinea pigs. The crude musk itself potentiated the effect of IsP but not that of salbutamol which is well known as a COMT-resistant .beta.-agonist. The .beta.-adrenergic potentiation induced by W in musk was very selective to cardiac muscle, and there may be other factors in musk which induce the .beta.-adrenergic potentiation in tracheal muscle, at least in part due to the COMT-inhibitory activity.