| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology and Biophysics, University of Washington, Seattle, Washington, United States
* To whom correspondence should be addressed. E-mail: santana{at}u.washington.edu.
By hyperpolarizing arterial smooth muscle, voltage-gated, calcium-independent potassium (Kv) channels decrease calcium influx and thus oppose constriction. However, the molecular nature of the Kv channels functional in arterial smooth muscle remains controversial. Recent investigations have emphasized a predominant role of Kv1 channels in regulating arterial tone. Here, we tested the hypothesis Kv2 channels may also significantly regulate tone of rat cerebral arteries. We found that Kv2.1 transcript and protein is present in cerebral arterial smooth muscle. In addition, our analysis indicates that a substantial component (about 50%) of the voltage-dependencies and kinetics of Kv currents in voltage-clamped cerebral arterial myocytes are consistent with Kv2 channels. Accordingly, we found that stromatoxin, a specific inhibitor of Kv2 channels, significantly decreased Kv currents in these cells. Furthermore, stromatoxin enhanced myogenic constriction of pressurized arterial segments. We also found that during angiotensin II-induced hypertension, Kv2 channel function was reduced in isolated myocytes and in intact arteries. This suggests that impaired Kv2 channel activity may contribute to arterial dysfunction during hypertension. Based on these novel observations, we propose a new model of Kv channel function in arterial smooth muscle in which Kv2 channels, in combination with Kv1 channels, contribute to membrane hyperpolarization and thus oppose constriction.
This article has been cited by other articles:
|
|
 |
|
  J. Layne, M. Werner, D. Hill-Eubanks, and M. Nelson NFATc3 regulates BK channel function in murine urinary bladder smooth muscle Am J Physiol Cell Physiol, September 1, 2008; 295(3): C611 - C623. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. F. Navedo, M. Nieves-Cintron, G. C. Amberg, C. Yuan, V. S. Votaw, W. J. Lederer, G. S. McKnight, and L. F. Santana AKAP150 Is Required for Stuttering Persistent Ca2+ Sparklets and Angiotensin II-Induced Hypertension Circ. Res., February 1, 2008; 102(2): e1 - e11. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. D. Luykenaar and D. G. Welsh Activators of the PKA and PKG pathways attenuate RhoA-mediated suppression of the KDR current in cerebral arteries Am J Physiol Heart Circ Physiol, June 1, 2007; 292(6): H2654 - H2663. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X.-L. Shi, G.-L. Wang, Z. Zhang, Y.-J. Liu, J.-H. Chen, J.-G. Zhou, Q.-Y. Qiu, and Y.-Y. Guan Alteration of Volume-Regulated Chloride Movement in Rat Cerebrovascular Smooth Muscle Cells During Hypertension Hypertension, June 1, 2007; 49(6): 1371 - 1377. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
