In the present study we investigated the effects of chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition. In rats subjected to chemical sympathectomizy with the neuro- toxin 6-hydroxydopamine (6-OHDA) we observed a significant increase of mast cell density, and in particular of degranulat- ing mast cells, suggesting a close relationship between the cardiac catecholaminergic system and mast cell activation. In parallel, chronic 6-OHDA treatment was associated with increased collagen deposition. The influence of the β-adren- ergic receptor component was investigated in rats subjected to chronic propranolol administration, that caused a further significant increase in mast cell activation associated with a lower extent of collagen deposition when compared to chem- ical sympathectomy. These data are the first demonstration of a close relationship between rat cardiac mast cell activation and the catecholaminergic system, with a complex interplay with cardiac collagen deposition. Specifically, abrogation of the cardiac sympathetic efferent drive by chemical sympathectomy causes mast cell activation and interstitial fibrosis, possibly due to the local effects of the neurotoxin 6-hydroxy- dopamine. In contrast, β-adrenergic blockade is associated with enhanced mast cell degranulation and a lower extent of collagen deposition in the normal myocardium. In conclusion, cardiac mast cell activation is influenced by β-adrenergic influences.
Correspondence: Rosanna Nano,
Department of Animal Biology, University of Pavia,
European Journal of Histochemistry
2006; vol. 50 issue 2 (Apr-Jun):133-140
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