The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice
Open accessAbstract
In addition to nitric oxide (NO) and prostacyclin (PGI 2 ), the endothelium generates the endothelium-derived hyperpolarizing factor (EDHF). We set out to determine whether an EDHF-like response can be detected in wild-type (WT) and endothelial NO synthase knockout mice (eNOS −/−) mice. Vasodilator responses to endothelium-dependent agonists were determined in vivo and in vitro. In vivo , bradykinin induced a pronounced, dose-dependent decrease in mean arterial pressure (MAP) which did not differ between WT and eNOS −/− mice and was unaffected by treatment with N ω -nitro- l -arginine methyl ester and diclofenac. In the saline-perfused hindlimb of WT and eNOS −/− mice, marked N ω -nitro- l -arginine ( l -NA, 300 μmol/liter)- and diclofenac-insensitive vasodilations in response to both bradykinin and acetylcholine (ACh) were observed, which were more pronounced than the agonist-induced vasodilation in the hindlimb of WT in the absence of l -NA. This endothelium-dependent, NO/PGI 2 -independent vasodilatation was sensitive to KCl (40 mM) and to the combination of apamin and charybdotoxin. Gap junction inhibitors (18α-glycyrrhetinic acid, octanol, heptanol) and CB-1 cannabinoid-receptor agonists (Δ 9 -tetrahydrocannabinol, HU210) impaired EDHF-mediated vasodilation, whereas inhibition of cytochrome P450 enzymes, soluble guanylyl cyclase, or adenosine receptors had no effect on EDHF-mediated responses. These results demonstrate that in murine resistance vessels the predominant agonist-induced endothelium-dependent vasodilation in vivo and in vitro is not mediated by NO, PGI 2 , or a cytochrome P450 metabolite, but by an EDHF-like principle that requires functional gap junctions.
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Cites
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H 2 S as a Physiologic Vasorelaxant: Hypertension in Mice with Deletion of Cystathionine γ-Lyase
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P-450 Metabolites of Arachidonic Acid in the Control of Cardiovascular Function
Roman, R. J. (2002) · Physiological Reviews · doi:10.1152/physrev.00021.2001 · Cited by 1,309
Endothelial dysfunction and vascular disease - a 30th anniversary update
Vanhoutte, P. M., Shimokawa, H., Feletou, M., & Tang, E. H. C. (2017) · Acta Physiologica · doi:10.1111/apha.12646 · Cited by 937
Self-citationEndothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture)
Félétou, M., & Vanhoutte, P. M. (2006) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00292.2006 · Cited by 818
Self-citationHydrogen peroxide is an endothelium-derived hyperpolarizing factor in mice
Matoba, T., Shimokawa, H., Nakashima, M., Hirakawa, Y., Mukai, Y., Hirano, K., Kanaide, H., & Takeshita, A. (2000) · Journal of Clinical Investigation · doi:10.1172/jci10506 · Cited by 722
Metadata
- Authors
- Brandes, R. P., Schmitz-Winnenthal, F.-H., Félétou, M., Gödecke, A., Huang, P. L., Vanhoutte, P. M., Fleming, I., & Busse, R.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2000-08-15
- Volume
- 97
- Issue
- 17
- Pages
- 9747-9752
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W1980975971
- Cited by
- 282
- References
- 32
- FWCI
- 11.34
- Type
- journal article
- Language
- en
- Open access
- green
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- Brandes, R. P., Schmitz-Winnenthal, F.-H., Félétou, M., Gödecke, A., Huang, P. L., Vanhoutte, P. M., Fleming, I., & Busse, R. (2000). An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.97.17.9747
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