Abstract
The contractibility of blood vessels depends on their normal structure and the availability of calcium ions; it changes under the influence of numerous contracting and relaxing factors, which control the activities of various pathways of intracellular and intercellular signaling. The main aim of the study was to investigate, by means of perfusion pressure in rat tail arteries, the role of Ca(2+) in vascular response to α-1 adrenoceptor activation by phenylephrine (PHE) and Bay K8644 agonist of the L-type calcium channel and caffeine before and after a post-mortem interval (PMI) of 2, 4, 6 and 8 h. A phasic increase of perfusion pressure in rat tail arteries, as induced by PHE or caffeine, in Ca(2+)-free solutions was used as an indicator of intracellular Ca(2+) release through the inositol 1,4,5-triphosphate and ryanodine receptor pathways, respectively. In Ca(2+)-free-ethylene glycol tetraacetic acid (EGTA)-poly(sodium styrenesulfonate) (PSS) and in Ca(2+)-EGTA-PSS, the PHE induced elevation of perfusion pressure significantly decreased. Vascular responses to caffeine (20 mmol/1) in Ca(2+)-free-EGTA-PSS, with an increase of PMI from 2-8 h, did not change significantly. A similar effect was observed with vascular responses to K...Continue Reading
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