Tetrandrine (Tet) 64 μM and verapamil (Ver) 8.4 μM relaxed the contraction of coronary artery strips. It is reversed by raising the extracellular Ca++ from 2.7 to 14.4 mM. Within a certain range (Tet 0. 1 μM 0.1 mM, Ver 1 nM 1 μM) the percentage of relaxation was in proportion to the dose. However, Tet and Ver exert no significant inhibition on the extracellular Ca++-dependent contraction induced by norepinephrine (NE). Probably Tet and Ver primarily inhibited the potential-dependent channel (PDC) and prevented the influx of Ca++ through PDC.
Tet 10 μM and Ver 0.1 μM also inhibited the release of intracellular Ca++ by NE. This shows that Tet and Ver might affect the transport of the intracellular Ca++. The relaxant effect of isoproterenol on the coronary strips was not blocked by Tet and Ver. Tet is therefore considered to be different from the β-blocker propranolol but similar to the calcium antagonist Ver.
This article reports the relationship between immunological genetic factor and the familial occurrence of hypertrophic cardiomyopathy by using HLA as marker of inheritance. 42 subjects (26 males, 16 females) of 6 families were investigated. 19 of them were found to have hypertrophie cardiomyopathy (obstructive 11, non-obstructive 8) confirmed by echocardiogram, with ages ranging from 29–68 years (average 43 years). HLA of the same subjects were studied, 4 families provided information of transmission by HLA antigens, and at least 2 family members were affected by hypertrophie cardiomyopathy. According to the HLA haplotype analysis in affected siblings, [the HLA haplotype of their parents has been shown to be nonrandom in distribution (x2 = 4.35,P < 0.05). Thus, there is certain correlation between the HLA haplotype and hypertrophie cardiomyopathy. Our findings show that genetic and familial factors may play an important role in the occurrence of the disease. Whether some HLA haplotype could afford some clue for the early diagnosis of this disease remains to be further investigated.