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Mechanisms underlying nitric oxide‐mediated modulation of vasoconstriction in small arteries
Author(s) -
Plane Frances,
Sandow Shaun L
Publication year - 2007
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.21.6.a1232
Subject(s) - vasoconstriction , mesenteric arteries , nitric oxide , chemistry , phenylephrine , basilar artery , endothelium , vasodilation , endocrinology , endothelium derived hyperpolarizing factor , medicine , anatomy , artery , charybdotoxin , blood pressure
Contractile activation of vascular smooth muscle cells is limited by the release of endothelium‐derived relaxing factors such as nitric oxide (NO). We have investigated the role of Ca 2+ ‐activated potassium channels (K Ca ) and inositol triphophate receptors (IP 3 R) in endothelium‐dependent modulation of vasoconstriction in rat basilar and mesenteric arteries. L‐N G ‐nitroarginine methyl ester (L‐NAME; 100 μM) or 1‐[(2‐chlorophenyl) diphenylmethyl]‐1H‐pyrazole (TRAM‐34; 5 μM), significantly potentiated contractions to 5‐hydroxytrptamine (5‐HT; 0.1 nM‐10 μM) and phenylephrine (PE; 0.01‐10 μM) in endothelium‐intact segments of rat basilar and mesenteric artery, respectively. The effects of L‐NAME and TRAM‐34 were not additive. Application of xestospongin (10 μM), a non‐selective IP 3 R antagonist, to the lumen of pressurized rat mesenteric arteries potentiated constrictions to PE to a greater extent than L‐NAME, and subsequent addition of either L‐NAME or TRAM‐34 did not cause further increase in PE‐evoked responses. Ultrastructural immunohistochemistry revealed an accumulation of IP 3 R within endothelial cell projections associated with myoendothelial gap junctions in these arteries. These data indicate that activation of endothelial intermediate conductance K Ca and IP 3 R may play a key role in NO‐dependent modulation of vasoconstriction in rat small arteries.