Franklin

a| 9781615043361 (electronic bk.)

z| 9781615043378 (pbk.)

a| 10.4199/C00032ED1V01Y201105ISP020 2| doi

a| (CaBNVSL)CDLLS201105ISP020

a| (CaBNVSL)201105ISP020

a| (PU)6198002-penndb-Voyager

a| CaBNVSL c| CaBNVSL d| CaBNVSL

a| QP88.45 b| .F454 2011 Part II

a| QS 532.5.E7 b| F454e 2011 Part II

a| 612.13 2| 22

a| Félétou, Michel, d| 1956- e| author

a| The endothelium. n| Part II, p| EDHF-mediated responses "The classical pathway" h| [electronic resource] / c| Michel Félétou.

a| EDHF-mediated responses "The classical pathway."

a| San Rafael, Calif. (1537 Fourth Street, San Rafael, CA 94901 USA) : b| Morgan and Claypool, c| c2011.

a| 1 electronic text (viii, 43, 139-291, 199 pages) : b| ill

a| text b| txt 2| rdacontent

a| computer b| c 2| rdamedia

a| online resource b| cr 2| rdacarrier

a| Integrated systems physiology, from molecule to function to disease, x| 2154-5626 ; v| # 20

a| Restricted for use by site license.

a| Also available in printing.

a| Mode of access: World Wide Web.

a| Part of: Colloquium digital library of life sciences.

a| Series from website.

a| Includes bibliographical references (pages 139-291).

a| 1. Endothelium-dependent hyperpolarizations: the classical "EDHF" pathway -- 1.1 The classical "EDHF" pathway: historical notes -- 1.2 Early characterization of EDHF-mediated responses -- 1.3 Identification and localization of the potassium channels involved in EDHF-mediated responses -- 1.4 Fundamental role of endothelial cell hyperpolarization -- 1.5 Beyond endothelial cell hyperpolarization -- 1.5.1 Myoendothelial gap junctions -- 1.5.2 Regulation of gap junction communication -- 1.5.3 Potassium ion accumulation in the intercellular space -- 1.5.3.1 Physiological evidence -- 1.5.3.2 Potassium cloud theory -- 1.6 Why two populations of endothelial potassium channels: SKca and IKca -- 1.6.1 SKca localization and postulated function -- 1.6.2 IKca localization and postulated function -- 1.6.3 Regulation of IKca and SKca activity -- 1.7 Lessons from genetically modified animals -- 1.7.1 NOS and COX genes -- 1.7.2 TRP channel genes -- 1.7.3 Potassium channel genes -- 1.7.4 Connexin genes -- 1.8 Physiological role of EDHF-mediated responses -- 1.8.1 EDHF-mediated responses and arterial blood pressure -- 1.8.2 Flow-mediated vasodilatation -- 1.8.3 Conducted vasodilatation -- 1.8.4 Vasomotion -- 1.8.5 Hypoxia -- 1.8.6 EDHF-mediated responses and gender -- 1.8.6.1 Sex hormones -- 1.8.6.2 Pregnancy -- 1.9 Cardiovascular diseases and alterations in EDHF-mediated responses -- 1.9.1 Impairment of EDHF-mediated responses -- 1.9.1.1 Hypertension -- 1.9.1.1.1 Genetic models of hypertension -- 1.9.1.1.2 Induced hypertension -- 1.9.1.1.3 Human hypertension and eclampsia -- 1.9.1.2 Aging -- 1.9.1.3 Diabetes -- 1.9.1.3.1 Insulin-dependent diabetes -- 1.9.1.3.2 Insulin-independent diabetes -- 1.9.1.4 Angioplasty -- 1.9.1.5 Transplantation -- 1.9.1.6 Sepsis -- 1.9.2 Enhancement of EDHF-mediated responses -- 1.9.2.1 Hypercholesterolemia and atherosclerosis -- 1.9.2.2 Diabetes -- 1.9.2.3 Ischemia-reperfusion -- 1.9.2.4 Heart failure -- 1.9.2.5 Hypertension -- 1.9.2.5.1 Renal circulation -- 1.9.2.5.2 NOS inhibition or deletion -- 1.9.2.5.3 Miscellaneous -- 1.10 Potential therapeutic interventions --

a| Conclusion -- References -- Author biography.

a| The endothelium controls vascular tone by releasing various vasoactive substances. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca2+ concentration of the endothelial cells followed by the opening of Ca2+-activated K+ channels of small and intermediate conductances (SKCa and IKCa). These channels show a distinct subcellular distribution, suggesting that their activation could be elicited by distinct stimuli. Following KCa activation, the endothelial hyperpolarization can be conducted to the underlying smooth muscle cells by electrical coupling through myo-endothelial gap junctions. In addition, the potassium efflux can lead to the accumulation of potassium ions in the intercellular space and the subsequent activation of smooth muscle Kir2.1 and/or Na+/K+-ATPase. The hyperpolarization of the smooth muscle cells produces vascular relaxation, predominantly by closing voltage-gated calcium channels, and vasodilatation. EDHF mediated responses are altered in various pathologies or, conversely, act as a compensating mechanism when other endothelial pathways are impaired. A better characterization of EDHF-mediated responses should allow determining whether or not new drugable targets can be identified within this endothelial pathway for the treatment of cardiovascular diseases.

a| Endothelium.

a| Endothelins.

a| Endothelium.

a| Endothelins.

a| Colloquium digital library of life sciences.

a| Colloquium series on integrated systems physiology, from molecule to function, x| 2154-5626 ; v| # 20.

u| http://hdl.library.upenn.edu/1017.12/1322771 z| Connect to full text