Role of EDHF in conduction of vasodilation along hamster cheek pouch arterioles in vivo
- 1 June 2000
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 278 (6), H1832-H1839
- https://doi.org/10.1152/ajpheart.2000.278.6.h1832
Abstract
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, ∼40 μm) was monitored at the site of application (local) and at 520 and 1,040 μm upstream (conducted). Under control conditions, ACh elicited local (22–65 μm) and conducted (14–44 μm) vasodilation. Indomethacin (10 μM) had no effect, whereasNω-nitro-l-arginine (100 μM) reduced local and conducted vasodilation by 5–8% (P < 0.05). Miconazole (10 μM) or 17-octadecynoic acid (17-ODYA; 10 μM) diminished local vasodilation by 15–20% and conducted responses by 50–70% (P < 0.05), suggesting a role for cytochromeP-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 Em, 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.Keywords
This publication has 39 references indexed in Scilit:
- Pentobarbital-sensitive EDHF comediates ACh-induced arteriolar dilation in the hamster microcirculation.American Journal of Physiology-Heart and Circulatory Physiology, 1999
- Endothelium-Derived Hyperpolarizing Factors and Vascular Cytochrome P450 Metabolites of Arachidonic Acid in the Regulation of ToneCirculation Research, 1999
- Epoxyeicosatrienoic acids, potassium channel blockers and endothelium‐dependent hyperpolarization in the guinea‐pig carotid arteryBritish Journal of Pharmacology, 1998
- Elevation of intracellular calcium in smooth muscle causes endothelial cell generation of NO in arteriolesProceedings of the National Academy of Sciences, 1997
- Role of activation of calcium-sensitive K+ channels in NO- and hypoxia-induced pial artery vasodilation.American Journal of Physiology-Heart and Circulatory Physiology, 1997
- Acetylcholine induces conducted vasodilation by nitric oxide-dependent and -independent mechanismsAmerican Journal of Physiology-Heart and Circulatory Physiology, 1997
- NO/PGI2‐independent vasorelaxation and the cytochrome P450 pathway in rabbit carotid arteryBritish Journal of Pharmacology, 1997
- Effects of cytochrome P450 inhibitors on potassium currents and mechanical activity in rat portal veinBritish Journal of Pharmacology, 1996
- Identification of Epoxyeicosatrienoic Acids as Endothelium-Derived Hyperpolarizing FactorsCirculation Research, 1996
- Characterization of acetylcholine-induced membrane hyperpolarization in endothelial cells.Circulation Research, 1992