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Cascade transmission in skeletal muscle arteries
Author(s) -
Kluess Heidi A
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1139.4
Subject(s) - ppads , phenylephrine , suramin , vasoconstriction , agonist , medicine , chemistry , endocrinology , receptor , blood pressure
Cascade transmission is the release of ATP from smooth muscle secondary to activation of the α 1 ‐adrenergic receptor and occurs in the skeletal muscle vasculature, but the functional significance is currently unknown. Femoral arteries from Fisher 344 female rats (2–3 months old) were prepared for wire myography. Phenylephrine (10 −5 M) was added and developed tension was recorded for 14 minutes (n=5). Following washing, either the P2 antagonists, PPADS or suramin or both were added 20 minutes prior to phenylephrine. In a subset of artery rings, phenylephrine was added a second time without blockers to ensure that phenylephrine‐mediated tension was not declining compared to the baseline phenylephrine. The hypothesis was that if cascade transmission contributed to α 1 ‐mediated vasoconstriction, then blocking P2 receptors would result in attenuation of developed tension. Tension was attenuated with PPADS (14±11%), suramin (23±10%) and both PPADS and suramin (32±16%)(p<0.05; all were different from phenylephrine only and double block attenuated more than PPADs). To assess whether this affect was specific to α 1 ‐mediated vasoconstriction, potassium chloride (60mM; n=3) was substituted for phenylephrine. PPADS and suramin did not attenuate potassium chloride‐mediated vasoconstriction. These data suggest that a portion of α 1 ‐mediated vasoconstriction is caused by cascade transmission.