Dystrophic hamsters exhibit increased vascular smooth muscle contractility to vasopressor amines, supporting the vascular hypothesis of muscular dystrophy.
No immediate clinical implications; supports vascular hypothesis of muscular dystrophy in dystrophic hamsters.
To investigate the "vascular" hypothesis of muscular dystrophy, the sensitivity and contractility of aortic spiral strips of dystrophic (BIO 14.6) and normal (FIB) hamsters have been determined to various smooth muscle agonists. The results obtained with cumulative dose-response curves show that there is no increase in the sensitivity of the dystrophic compared with the normal aorta to noradrenaline, phenylephrine, isoproterenol, histamine, or 5-hydroxytryptamine. However, there was a significant increase in the force generated by aortic strips of the dystrophic animals to all agonists. Determination of noncollagen and collagen protein showed that there was no difference in the relative proportions of these proteins in the aortas from the two strains. The results show that in this animal model of dystrophy an increased response to vasopressor amines occurs and is in accordance with that expected of the vascular hypothesis.
No takes yet. Share an insight, caveat, or question.
Hunter et al. (1983) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: