The effect of long-term administration of ?1-blocker prazosin on capillary density in cardiac and skeletal muscle

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Abstract
The effect of prazosin on heart and muscle blood flow and capillary density was studied in rats. In acute experiments, α 1-blocker prazosin almost trebled blood flow in fast skeletal muscles [tibialis anterior (TA) and extensor digitorum longus (EDL)], but did not affect coronary flow when infused i.v. at a dose of 0.5 μg · ml−1 · min−1 for 30 min. Prazosin in an equivalent dose was then given orally over a period of 5 weeks to investigate its effect on capillarisation in heart and skeletal muscle. Capillary density (CD, capillaries · mm−2), estimated in frozen sections stained for alkaline phosphatase, was similar in the hearts of prazosin-treated and control rats. Capillary/fibre ratio in skeletal muscles increased from 1.52±0.019 in control EDL to 1.69±0.01 (PPPP<0.005). Unilateral crush of the lateral peroneal nerve and subsequent reinnervation over the next 7 weeks resulted in redistribution of fibre types from a typical mosaic pattern into groups composed of fibres of similar oxidative capacity. Capillary density as well as capillary/fibre ratio in purely glycolytic areas was lower when compared to supply of glycolytic fibres in normal muscles. Oral administration of prazosin over the whole period of reinnervation not only maintained the original level of capillarity associated with fast glycolytic fibres in control muscles, but considerably increased it. Thus long-term prazosin administration not only causes an increase in capillary supply in normal muscles but also prevents loss of capillaries during reinnervation. The fact that it only increases capillarisation in tissues where it increases flow further supports the hypothesis that capillary growth can be initiated by mechanical factors connected with high blood flow.