Premium
FUNCTIONAL VASODILATION IN THE RAT SPINOTRAPEZIUS MUSCLE: ROLE OF NITRIC OXIDE, PROSTANOIDS AND EPOXYEICOSATRIENOIC ACIDS
Author(s) -
Xiang Lusha,
Naik Jay S,
Hester Robert L
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04864.x
Subject(s) - nitric oxide , vasodilation , chemistry , epoxyeicosatrienoic acid , medicine , endocrinology , pharmacology , biochemistry , arachidonic acid , enzyme
SUMMARY1 The present study was designed to determine the mechanisms responsible for functional vasodilation of arterioles paired and unpaired with venules in the rat spinotrapezius muscle. 2 The spinotrapezius muscle (from Sprague‐Dawley rats) was treated with combinations of the nitric oxide synthase inhibitor N G ‐nitro‐ l‐ arginine methyl ester ( l ‐NAME; 100 mmol/L), the cyclo‐oxygenase inhibitor indomethacin (10 mmol/L) and the epoxygenase inhibitor 6‐(2‐propargyloxyphenyl) hexanoic acid (PPOH; 30 mmol/L) to determine vascular responses to muscle stimulation. Both paired and unpaired arcade arterioles were chosen for microcirculatory observation. Arteriolar diameter was measured following 2 min muscle stimulation before and 30 min after subsequent application of each inhibitor. 3 In all cases, l ‐NAME treatment resulted in decreased basal diameter that was restored to control levels by the addition of sodium nitroprusside (0.01–0.1 mmol/L) to the superfusion solution. N G ‐Nitro‐ l‐ arginine methyl ester significantly inhibited the functional dilation in both paired (–20 ± 3%) and unpaired (–29 ± 3%) arterioles, whereas these inhibitory effects of l ‐NAME were diminished after pretreatment with indomethacin and PPOH. Indomethacin treatment attenuated the dilation in paired (–33 ± 5%) but not unpaired (–6 ± 4%) arterioles. Treatment with PPOH had no effect on the functional dilation in either set of arterioles. Approximately 50% of the vasodilatory responses remained in the presence of l ‐NAME, indomethacin and PPOH. 4 These results suggest that both nitric oxide and vasodilator prostanoid(s) are involved in mediating functional vasodilation in the rat spinotrapezius. The vasodilator prostanoid(s) released from venules is responsible for a portion of the vasodilation of the paired arteriole. The results also suggest possible interactions between the synthesis of nitric oxide and prostaglandin or epoxyeicosatrienoic acids during muscle contraction.