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This Article Full Text (PDF) Free All Versions of this Article: 102/5/2080    most recent 00002.2007v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Robertson, T. P. Search for Related Content PubMed Articles by Robertson, T. P.

LETTER TO THE EDITOR

Last Word on Point:Counterpoint "Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained HPV"

Drs. Madden and Packer (2) both intimate that one possible explanation for the loss of HPV following endothelial denudation could be that some experimentalists damage the underlying smooth muscle during the denudation process. However, it has been reported several times that denudation eliminates sustained HPV, whereas smooth muscle-specific contractile responses, such as potassium-induced depolarization, are unaffected (e.g., Ref. 4).

Indeed, when considering potential "damage" to smooth muscle and the resultant effects on function, I would concur with Dr. Wadsworth (2) when posing the question as to whether enzymatically dispersed cells in culture are behaving normally?

Dr. Wadsworth makes a case for sustained HPV being the result of an inhibition of the release of endothelium-derived nitric oxide by hypoxia. As with many aspects of HPV, there is evidence both for and against this hypothesis. However, the balance of data seems to tip against this possibility, and it is more probable that NO may be increased in HPV rather than decreased (discussed in Ref. 1).

Drs. Meldrum, Lahn, and Yuan (2) seek to bring an accord to the current debate by suggesting that HPV is comprised of a concert of inter- and intradependent signal transduction pathways acting in a harmonious fashion to elicit the desired contractile response. At this point, we must put this notion in the context of the Point:Counterpoint debate, which is to avoid objectivity and be completely subjective. Objectively, I concur with Drs. Meldrum, Lahn, and Yuan and agree that HPV is most certainly a well orchestrated multi-factorial process. Subjectively, it's the endothelium, dummy!

FOOTNOTES

Address for reprint requests and other correspondence: T. P. Robertson, Univ. of Georgia, Athens, GA 30605 (e-mail: troberts{at}vet.uga.edu)

REFERENCES

1. Aaronson PI, Robertson TP, Ward JPT. Endothelium-derived mediators and hypoxic pulmonary vasoconstriction. Resp Physiol Neurobiol 132: 107–120, 2002.[CrossRef]
2. Madden JA, Wadsworth RM, Meldrum DR, Lahm T, Yuan J, Packer CS, Pelaez NJ. Comments on Point:Counterpoint: Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained HPV. J Appl Physiol. In press.
3. Rochefort GY, Michelakis ED. Counterpoint: Release of an endothelium-derived vasoconstrictor and Rhoa/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are not the main effectors for full and sustained HPV. J Appl Physiol. In press.
4. Robertson TP, Aaronson PI, Ward JPT. Ca²⁺ sensitization during sustained hypoxic pulmonary vasoconstriction is endothelium dependent. Am J Physiol Lung Cell Mol Physiol 284: L1121–L1126, 2003.[Abstract/Free Full Text]

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