| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology, University of Maryland, Baltimore, Md, USA
* To whom correspondence should be addressed. E-mail: jmauban{at}umaryland.edu.
The possible roles of endothelial [Ca2+]i, nitric oxide (NO), arachidonic acid (AA)
metabolites, and Ca2+-activated K+ channels (KCa) in adrenergically-induced vasomotion were examined in pressurized rat mesenteric arteries. Removal of the endothelium or buffering [Ca2+]i selectively in endothelial cells (EC) with BAPTA eliminated vasomotion in response to phenylephrine (PE, 10.0 µM). In arteries with intact
endothelium, inhibition of NO synthase with N
-nitro-L-arginine methyl ester (LNAME,
300.0 µM) or N-nitro-L-arginine (L-NNA, 300.0 µM) did not eliminate vasomotion. Neither inhibition of cGMP formation with 10.0 µM 1H-
[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) nor inhibition of prostanoid formation (indomethacin, 10.0µM) eliminated vasomotion. Similarly, inhibition of AA cyt P450 metabolism with intraluminal application of 17-octadecynoic acid (17-ODYA) or 6-(2- propargyloxyphenyl) hexanoic acid (PPOH) failed to eliminate vasomotion. In contrast, intraluminal application of the KCa channel blockers apamin (250.0 nM) and charybdotoxin (100.0 nM), together, abolished vasomotion and changed synchronous
Ca2+ oscillations in SMC to asynchronous propagating Ca2+ waves. Apamin, charybdotoxin, or iberiotoxin (100.0 nM) alone did not eliminate vasomotion, nor did the combination of apamin and iberiotoxin. The results show that adrenergic vasomotion in
rat mesenteric arteries is critically dependent on Ca2+-activated K+ channels in endothelial cells. Since these channels (SKCa and IKCa) are a recognized component of endotheliumderived hyperpolarizing factor (EDHF), we conclude therefore that EDHF is essential for
the development of adrenergically-induced vasomotion.
This article has been cited by other articles:
|
|
 |
|
  J. C. B. Jacobsen, C. Aalkjaer, V. V Matchkov, H. Nilsson, J. J Freiberg, and N.-H. Holstein-Rathlou Heterogeneity and weak coupling may explain the synchronization characteristics of cells in the arterial wall Phil Trans R Soc A, October 13, 2008; 366(1880): 3483 - 3502. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. S. Silva, A. Kapela, and N. M. Tsoukias A mathematical model of plasma membrane electrophysiology and calcium dynamics in vascular endothelial cells Am J Physiol Cell Physiol, July 1, 2007; 293(1): C277 - C293. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. C. B. Jacobsen, C. Aalkjaer, H. Nilsson, V. V. Matchkov, J. Freiberg, and N.-H. Holstein-Rathlou Activation of a cGMP-sensitive calcium-dependent chloride channel may cause transition from calcium waves to whole cell oscillations in smooth muscle cells Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H215 - H228. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. E. Haddock, T. H. Grayson, T. D. Brackenbury, K. R. Meaney, C. B. Neylon, S. L. Sandow, and C. E. Hill Endothelial coordination of cerebral vasomotion via myoendothelial gap junctions containing connexins 37 and 40 Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2047 - H2056. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-L. Beny, M. Koenigsberger, and R. Sauser Role of myoendothelial communication on arterial vasomotion Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2036 - H2038. [Full Text] [PDF]
|
|
|
|
|
|
V. V. Matchkov, A. Rahman, L. M. Bakker, T. M. Griffith, H. Nilsson, and C. Aalkjaer Analysis of effects of connexin-mimetic peptides in rat mesenteric small arteries Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H357 - H367. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. E Haddock and C. E Hill Rhythmicity in arterial smooth muscle J. Physiol., August 1, 2005; 566(3): 645 - 656. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
