Maximum shortening velocity of lymphatic muscle approaches that of striated muscle
Identifieur interne : 002B87 ( Pmc/Curation ); précédent : 002B86; suivant : 002B88Maximum shortening velocity of lymphatic muscle approaches that of striated muscle
Auteurs : Rongzhen Zhang [États-Unis] ; Anne I. Taucer [États-Unis] ; Anatoliy A. Gashev [États-Unis] ; Mariappan Muthuchamy [États-Unis] ; David C. Zawieja [États-Unis] ; Michael J. Davis [États-Unis]Source :
- American Journal of Physiology - Heart and Circulatory Physiology [ 0363-6135 ] ; 2013.
Abstract
Lymphatic muscle (LM) is widely considered to be a type of vascular smooth muscle, even though LM cells uniquely express contractile proteins from both smooth muscle and cardiac muscle. We tested the hypothesis that LM exhibits an unloaded maximum shortening velocity (
Url:
DOI: 10.1152/ajpheart.00898.2012
PubMed: 23997104
PubMed Central: 3840257
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<series><title level="j">American Journal of Physiology - Heart and Circulatory Physiology</title>
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<front><div type="abstract" xml:lang="en"><p>Lymphatic muscle (LM) is widely considered to be a type of vascular smooth muscle, even though LM cells uniquely express contractile proteins from both smooth muscle and cardiac muscle. We tested the hypothesis that LM exhibits an unloaded maximum shortening velocity (<italic>V</italic>
<sub>max</sub>
) intermediate between that of smooth muscle and cardiac muscle. Single lymphatic vessels were dissected from the rat mesentery, mounted in a servo-controlled wire myograph, and subjected to isotonic quick release protocols during spontaneous or agonist-evoked contractions. After maximal activation, isotonic quick releases were performed at both the peak and plateau phases of contraction. <italic>V</italic>
<sub>max</sub>
was 0.48 ± 0.04 lengths (<italic>L</italic>
)/s at the peak: 2.3 times higher than that of mesenteric arteries and 11.4 times higher than mesenteric veins. In cannulated, pressurized lymphatic vessels, shortening velocity was determined from the maximal rate of constriction [rate of change in internal diameter (−d<italic>D</italic>
/d<italic>t</italic>
)] during spontaneous contractions at optimal preload and minimal afterload; peak −d<italic>D</italic>
/d<italic>t</italic>
exceeded that obtained during any of the isotonic quick release protocols (2.14 ± 0.30 <italic>L</italic>
/s). Peak −d<italic>D</italic>
/d<italic>t</italic>
declined with pressure elevation or activation using substance P. Thus, isotonic methods yielded <italic>V</italic>
<sub>max</sub>
values for LM in the mid to high end (0.48 <italic>L</italic>
/s) of those the recorded for phasic smooth muscle (0.05–0.5 <italic>L</italic>
/s), whereas isobaric measurements yielded values (>2.0 <italic>L</italic>
/s) that overlapped the midrange of values for cardiac muscle (0.6–3.3 <italic>L</italic>
/s). Our results challenge the dogma that LM is classical vascular smooth muscle, and its unusually high <italic>V</italic>
<sub>max</sub>
is consistent with the expression of cardiac muscle contractile proteins in the lymphatic vessel wall.</p>
</div>
</front>
</TEI>
<pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Am J Physiol Heart Circ Physiol</journal-id>
<journal-id journal-id-type="iso-abbrev">Am. J. Physiol. Heart Circ. Physiol</journal-id>
<journal-id journal-id-type="hwp">ajpheart</journal-id>
<journal-id journal-id-type="pmc">ajpheart</journal-id>
<journal-id journal-id-type="publisher-id">AJPHEART</journal-id>
<journal-title-group><journal-title>American Journal of Physiology - Heart and Circulatory Physiology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0363-6135</issn>
<issn pub-type="epub">1522-1539</issn>
<publisher><publisher-name>American Physiological Society</publisher-name>
<publisher-loc>Bethesda, MD</publisher-loc>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23997104</article-id>
<article-id pub-id-type="pmc">3840257</article-id>
<article-id pub-id-type="publisher-id">H-00898-2012</article-id>
<article-id pub-id-type="doi">10.1152/ajpheart.00898.2012</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Vascular Biology and Microcirculation</subject>
</subj-group>
</article-categories>
<title-group><article-title>Maximum shortening velocity of lymphatic muscle approaches that of striated muscle</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Rongzhen</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Taucer</surname>
<given-names>Anne I.</given-names>
</name>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Gashev</surname>
<given-names>Anatoliy A.</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Muthuchamy</surname>
<given-names>Mariappan</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zawieja</surname>
<given-names>David C.</given-names>
</name>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
</contrib>
<contrib contrib-type="author" corresp="yes"><name><surname>Davis</surname>
<given-names>Michael J.</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
</contrib>
<aff id="aff1"><sup>1</sup>
Department of Pathology, University of Texas Medical School, Houston, Texas;</aff>
<aff id="aff2"><sup>2</sup>
Department of Biomedical Engineering, Texas A&M University, College Station, Texas;</aff>
<aff id="aff3"><sup>3</sup>
Department of Medical Physiology, Texas A&M Health Science Center, Temple, Texas; and</aff>
<aff id="aff4"><sup>4</sup>
Department of Medical Pharmacology and Physiology, University of Missouri School of Medicine, Columbia, Missouri</aff>
</contrib-group>
<author-notes><corresp id="cor1">Address for reprint requests and other correspondence: M. J. Davis, <addr-line>Dept. of Medical Pharmacology and Physiology, Univ. of Missouri School of Medicine, 1 Hospital Dr., Rm. M451, Columbia, MO 65212</addr-line>
(e-mail: <email>davismj@health.missouri.edu</email>
).</corresp>
</author-notes>
<pub-date pub-type="epub"><day>30</day>
<month>8</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><day>15</day>
<month>11</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>15</day>
<month>11</month>
<year>2014</year>
</pub-date>
<pmc-comment> PMC Release delay is 12 months and
0 days and was based on the . </pmc-comment>
<volume>305</volume>
<issue>10</issue>
<fpage>H1494</fpage>
<lpage>H1507</lpage>
<history><date date-type="received"><day>5</day>
<month>12</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>27</day>
<month>8</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2013 the American Physiological Society</copyright-statement>
<copyright-year>2013</copyright-year>
<copyright-holder>American Physiological Society</copyright-holder>
</permissions>
<self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zh402213001494.pdf"></self-uri>
<abstract><p>Lymphatic muscle (LM) is widely considered to be a type of vascular smooth muscle, even though LM cells uniquely express contractile proteins from both smooth muscle and cardiac muscle. We tested the hypothesis that LM exhibits an unloaded maximum shortening velocity (<italic>V</italic>
<sub>max</sub>
) intermediate between that of smooth muscle and cardiac muscle. Single lymphatic vessels were dissected from the rat mesentery, mounted in a servo-controlled wire myograph, and subjected to isotonic quick release protocols during spontaneous or agonist-evoked contractions. After maximal activation, isotonic quick releases were performed at both the peak and plateau phases of contraction. <italic>V</italic>
<sub>max</sub>
was 0.48 ± 0.04 lengths (<italic>L</italic>
)/s at the peak: 2.3 times higher than that of mesenteric arteries and 11.4 times higher than mesenteric veins. In cannulated, pressurized lymphatic vessels, shortening velocity was determined from the maximal rate of constriction [rate of change in internal diameter (−d<italic>D</italic>
/d<italic>t</italic>
)] during spontaneous contractions at optimal preload and minimal afterload; peak −d<italic>D</italic>
/d<italic>t</italic>
exceeded that obtained during any of the isotonic quick release protocols (2.14 ± 0.30 <italic>L</italic>
/s). Peak −d<italic>D</italic>
/d<italic>t</italic>
declined with pressure elevation or activation using substance P. Thus, isotonic methods yielded <italic>V</italic>
<sub>max</sub>
values for LM in the mid to high end (0.48 <italic>L</italic>
/s) of those the recorded for phasic smooth muscle (0.05–0.5 <italic>L</italic>
/s), whereas isobaric measurements yielded values (>2.0 <italic>L</italic>
/s) that overlapped the midrange of values for cardiac muscle (0.6–3.3 <italic>L</italic>
/s). Our results challenge the dogma that LM is classical vascular smooth muscle, and its unusually high <italic>V</italic>
<sub>max</sub>
is consistent with the expression of cardiac muscle contractile proteins in the lymphatic vessel wall.</p>
</abstract>
<kwd-group><kwd>isometric</kwd>
<kwd>isotonic quick release</kwd>
<kwd>maximum shortening velocity</kwd>
<kwd>force-velocity</kwd>
<kwd>slack test</kwd>
<kwd>spontaneous contraction</kwd>
</kwd-group>
</article-meta>
</front>
</pmc>
</record>
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