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Letters to the Editor |
Letter to the Editor
Role of Kv1 Channels in Control of Arterial Myogenic Reactivity to Intraluminal Pressure
The Smooth Muscle Research Group, University of Calgary, Canada
To the Editor:
The recent Letter to the Editor from Drs D.J. Beech, A. Cheong, and N.J. Rusch1 regarding our article "Heteromultimeric Kv1 Channels Contribute to Myogenic Control of Arterial Diameter" in the February 4, 2005 issue of Circulation Research (Plane et al2) raises several important issues that we feel warrant clarification.
We wish to thank Beech and coauthors1 for their interest in our work and especially for pointing out several errors in the literature citations in the article. We sincerely apologize for any inconvenience that these errors may have caused our readers.
We agree with the general statement advanced by Beech and coauthors1 that our article "adds to an expanding body of evidence suggesting pivotal roles of the voltage-gated potassium channels in vascular smooth muscle cells as regulators of arterial tone" and that the role of these channels is an "emerging and important aspect of vascular biology". However, we strongly disagree with their contention that we erroneously claimed to have provided the first evidence that Kv1 channels play a role in controlling arterial myogenic reactivity to intraluminal pressure, the so-called "Bayliss effect," that is critical for appropriate regulation of blood pressure and organ-specific blood flow.
To demonstrate a role for Kv1 channels in the control of arterial myogenic reactivity, vessel diameter over a range of intraluminal pressures must be measured in the absence and presence of Kv1 channel inhibition. This is required to determine whether Kv1 channel inhibition causes a pressure-dependent increase in tone development, which would be expected if the channels contribute to control of myogenic contraction. The 3 articles cited by Beech and coauthors1 (ie, Albarwani et al3 and Cheong et al4,5) as examples of prior publications demonstrating the concept that Kv1 channels contribute to the control of arterial myogenic reactivity did not perform this critical experiment. These studies do show, however, that Kv1 channel inhibition in partially depolarized cerebral resistance vessels, pressurized to a single value of 60 mm Hg3 or exposed to endothelin-1 to simulate pressure-induced depolarization,4,5 causes further depolarization and/or constriction.3,4,5 The data are consistent with the view that Kv1 channels are active and contribute to membrane conductance of smooth muscle cells in the conditions used. However, because the effect of Kv1 channel inhibition was not assessed over a range of intraluminal pressures, no conclusions may be made regarding the role Kv1 channels in controlling arterial myogenic reactivity. In contrast, our study demonstrated that inhibition of Kv1 channels caused a pressure-dependent increase in vasoconstriction between 40 and 120 mm Hg in fourth-order rat-mesenteric resistance arteries and development of pressure-induced tone in apparently nonmyogenic second-order conduit vessels.2 Thus, our study does indeed provide the first evidence that Kv1 channels play a role in the myogenic response of arteries to alterations in intraluminal pressure.
Beech and coauthors1 also felt that we did not appropriately address "a potential discrepancy" between our data showing decreased Kv1 mRNA expression in myogenically active fourth order compared with nonmyogenic first and second order mesenteric arteries and previous publications showing a greater level of Kv1 transcript expression in rat6 and murine7 mesenteric arteries compared with aorta (note that Cox, Folander, and Swanson6 and not Cox, Lozinskaya, and Dietz8 should have been cited by Beech and coauthors1 for the rat transcript data). In this case, we believed that it was prudent not to speculate beyond the limits of the available data, because we did not determine the levels of aortic Kv1 transcripts, and neither Cox et al6 nor Fountain et al,8 examined mesenteric arteries of varied diameters and myogenic reactivity.
The errors in referencing highlighted by Beech and coauthors are addressed in a separate correction.9
References
- Beech DJ, Cheong A, Rusch NJ. Regulation of arterial tone by Kv1 potassium channels. Circ Res. 2005; 96: e58.
[Free Full Text] - Plane F, Johnson R, Kerr P, Wiehler W, Thorneloe K, Ishii K, Chen T, Cole W. Heteromultimeric Kv1 channels contribute to myogenic control of arterial diameter. Circ Res. 2005; 96: 216–224.
[Abstract/Free Full Text] - Albarwani S, Nemetz LT, Madden JA, Tobin AA, England SK, Pratt PF, Rusch NJ. Voltage-gated K+ channels in rat small cerebral arteries: Molecular identity of the functional channels. J Physiol (Lond). 2003; 551: 751–763.
[Abstract/Free Full Text] - Cheong A, Dedman AM, Xu SZ, Beech DJ. Kv
1 channels in murine arterioles: differential expression and regulation of diameter. Am J Physiol Heart Circ Physiol. 2001; 281: H1087–H1065.
- Cheong A, Dedman AM, Beech DJ. Expression and function of native potassium channel (Kv1) subunits in terminal arterioles of rabbit. J Physiol (Lond). 2001; 534: 691–700.
[Abstract/Free Full Text] - Cox RH, Folander K, Swanson R. Differential expression of voltage-gated K+ channel genes in arteries from spontaneously hypertensive and Wistar-Kyoto rats. Hypertens. 2001; 37: 1315–1322.
[Abstract/Free Full Text] - Fountain SJ, Cheong A, Flemming R, Mair L, Sivaprasadarao A, Beech DJ. Functional up-regulation of KCNA gene family expression in murine mesenteric resistance artery smooth muscle. J Physiol (Lond). 2004; 556: 29–42.
[Abstract/Free Full Text] - Cox RH, Lozinskaya IM, Dietz NJ. Differences in K+ current components in mesenteric artery myocytes from WKY and SHR. Am J Hypertens. 2001; 14: 897–907.[CrossRef][Medline] [Order article via Infotrieve]
- Plane F, Johnson R, Kerr P, Wiehler W, Thorneloe K, Ishii K, Chen T, Cole W. Heteromultimeric Kv1 channels contribute to myogenic control of arterial diameter (Correction). Circ Res. 2005; 97: e3.
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