Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 278, Issue 6, Pages H1832-H1839Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2000.278.6.H1832
Keywords
acetylcholine; endothelium-derived hyperpolarizing factor; cell-to-cell communication; cytochrome P-450 pathway; membrane potential; microcirculation; nitric oxide
Funding
- NHLBI NIH HHS [R01-HL-41026, R01-HL-56786] Funding Source: Medline
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We tested whether local and conducted responses to ACh depend on factors released from endothelial cells (EC) in cheek pouch arterioles of anesthetized hamsters. ACh was delivered from a micropipette (1 s, 500 nA), while arteriolar diameter (rest, similar to 40 mu m) was monitored at the site of application (local) and at 520 and 1,040 mu m upstream (conducted). Under control conditions, ACh elicited local (22-65 mu m) and conducted (14-44 mu m) vasodilation. Indomethacin (10 mu M) had no effect, whereas N-omega-nitro-L-arginine (100 mu M) reduced local and conducted vasodilation by 5-8% (P< 0.05). Miconazole (10 mu M) or 17-octadecynoic acid (17-ODYA; 10 mu M) diminished local vasodilation by 15-20% and conducted responses by 50-70% (P< 0.05), suggesting a role for cytochrome P-450 (CYP) metabolites in arteriolar responses to ACh. Membrane potential (Em) was recorded in smooth muscle cells (SMC) and in EC identified with dye labeling. At rest (control E-m, typically -30 mV), ACh evoked local (15-32 mV) and conducted (6-31 mV) hyperpolarizations in SMC and EC. Miconazole inhibited SMC and EC hyperpolarization, whereas 17-ODYA inhibited hyperpolarization of SMC but not of EC. Findings indicate that ACh-induced release of CYP metabolites from arteriolar EC evoke SMC hyperpolarization that contributes substantively to conducted vasodilation.
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