Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle
There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset of exercise is attributable to vasodilatation as...
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Veröffentlicht in: | The Journal of physiology 2004-06, Vol.557 (3), p.1013-1020 |
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description | There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting
this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset
of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis
we examined the blood flow response to a brief tetanic contraction in which potassium (K + ) was infused intra-arterially to elevate the [K + ] o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs
control contractions increased hindlimb blood flow by 97 ± 14 ml min â1 . During K + infusion the hyperaemic response to contraction was 8 ± 3 ml min â1 . Since the hindlimb blood flow was reduced during K + infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion
the hyperaemic response to contraction was preserved (89 ± 23 ml min â1 ). Recovery contractions performed after the discontinuation of the K + infusion elicited blood flow responses similar to control (100 ± 11 ml min â1 ). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs ( n = 6) K + infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation,
there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible
for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single
muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization. |
doi_str_mv | 10.1113/jphysiol.2004.062836 |
format | Article |
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this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset
of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis
we examined the blood flow response to a brief tetanic contraction in which potassium (K + ) was infused intra-arterially to elevate the [K + ] o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs
control contractions increased hindlimb blood flow by 97 ± 14 ml min â1 . During K + infusion the hyperaemic response to contraction was 8 ± 3 ml min â1 . Since the hindlimb blood flow was reduced during K + infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion
the hyperaemic response to contraction was preserved (89 ± 23 ml min â1 ). Recovery contractions performed after the discontinuation of the K + infusion elicited blood flow responses similar to control (100 ± 11 ml min â1 ). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs ( n = 6) K + infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation,
there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible
for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single
muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1113/jphysiol.2004.062836</identifier><identifier>PMID: 15073277</identifier><language>eng</language><publisher>9600 Garsington Road , Oxford , OX4 2DQ , UK: The Physiological Society</publisher><subject>Animals ; Blood Pressure - physiology ; Cell Polarity - physiology ; Dogs ; Electrophysiology ; Female ; Hindlimb - blood supply ; Hyperemia - physiopathology ; In Vitro Techniques ; Male ; Muscle Contraction - physiology ; Muscle, Skeletal - blood supply ; Muscle, Skeletal - physiopathology ; Potassium - pharmacology ; Regional Blood Flow - physiology ; Research Papers ; Vasodilation - physiology</subject><ispartof>The Journal of physiology, 2004-06, Vol.557 (3), p.1013-1020</ispartof><rights>2004 The Journal of Physiology © 2004 The Physiological Society</rights><rights>The Physiological Society 2004 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5524-f081972f354d6121a18b7a51641e1ea1b4fe9a22ed747514114844c0cd6e14c3</citedby><cites>FETCH-LOGICAL-c5524-f081972f354d6121a18b7a51641e1ea1b4fe9a22ed747514114844c0cd6e14c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665148/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1665148/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15073277$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hamann, Jason J.</creatorcontrib><creatorcontrib>Buckwalter, John B.</creatorcontrib><creatorcontrib>Clifford, Philip S.</creatorcontrib><title>Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting
this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset
of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis
we examined the blood flow response to a brief tetanic contraction in which potassium (K + ) was infused intra-arterially to elevate the [K + ] o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs
control contractions increased hindlimb blood flow by 97 ± 14 ml min â1 . During K + infusion the hyperaemic response to contraction was 8 ± 3 ml min â1 . Since the hindlimb blood flow was reduced during K + infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion
the hyperaemic response to contraction was preserved (89 ± 23 ml min â1 ). Recovery contractions performed after the discontinuation of the K + infusion elicited blood flow responses similar to control (100 ± 11 ml min â1 ). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs ( n = 6) K + infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation,
there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible
for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single
muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.</description><subject>Animals</subject><subject>Blood Pressure - physiology</subject><subject>Cell Polarity - physiology</subject><subject>Dogs</subject><subject>Electrophysiology</subject><subject>Female</subject><subject>Hindlimb - blood supply</subject><subject>Hyperemia - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Muscle Contraction - physiology</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Muscle, Skeletal - physiopathology</subject><subject>Potassium - pharmacology</subject><subject>Regional Blood Flow - physiology</subject><subject>Research Papers</subject><subject>Vasodilation - physiology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcuO1DAQRS0EYnoG_gAhrxCbNC4_4mSDhEYwgEaCRQuJleV2Kh0PTtzYCaP8PWmlee1YeVH3HlfpEPIM2BYAxKu7YzdnH8OWMya3rOSVKB-QDciyLrSuxUOyYYzzQmgFF-Qy5zvGQLC6fkwuQDEtuNYb8vWLzbHxwY529HGgPtO4D_5gx5hm2sZEXRzGZN1pWvihmRw2tJuPmCz23lI_UGcHPyDN3zDgaAPtp-wCPiGPWhsyPj2_V2T37u3u-n1x--nmw_Wb28IpxWXRsgpqzVuhZFMCBwvVXlsFpQQEtLCXLdaWc2y0XC6RALKS0jHXlAjSiSvyesUep32PjcPTtsEck-9tmk203vw7GXxnDvGHgbJccNUCeHEGpPh9wjya3meHIdgB45SN5oxDXaolKNegSzHnhO3vT4CZkxLzS4k5KTGrkqX2_O8F_5TODpZAtQbufcD5v6Bm9_Ezr-RSfblWO3_o7n1Cs4ZzdB7H2SiljVhIIMRPYIGsSg</recordid><startdate>20040615</startdate><enddate>20040615</enddate><creator>Hamann, Jason J.</creator><creator>Buckwalter, John B.</creator><creator>Clifford, Philip S.</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040615</creationdate><title>Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle</title><author>Hamann, Jason J. ; Buckwalter, John B. ; Clifford, Philip S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5524-f081972f354d6121a18b7a51641e1ea1b4fe9a22ed747514114844c0cd6e14c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Animals</topic><topic>Blood Pressure - physiology</topic><topic>Cell Polarity - physiology</topic><topic>Dogs</topic><topic>Electrophysiology</topic><topic>Female</topic><topic>Hindlimb - blood supply</topic><topic>Hyperemia - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Muscle Contraction - physiology</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Muscle, Skeletal - physiopathology</topic><topic>Potassium - pharmacology</topic><topic>Regional Blood Flow - physiology</topic><topic>Research Papers</topic><topic>Vasodilation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hamann, Jason J.</creatorcontrib><creatorcontrib>Buckwalter, John B.</creatorcontrib><creatorcontrib>Clifford, Philip S.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hamann, Jason J.</au><au>Buckwalter, John B.</au><au>Clifford, Philip S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>2004-06-15</date><risdate>2004</risdate><volume>557</volume><issue>3</issue><spage>1013</spage><epage>1020</epage><pages>1013-1020</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>There is a rapid increase in blood flow to active skeletal muscle with the onset of exercise, but the mechanism(s) eliciting
this increase remains elusive. We hypothesized that the rapid increase in blood flow to active skeletal muscle with the onset
of exercise is attributable to vasodilatation as a consequence of smooth muscle hyperpolarization. To test this hypothesis
we examined the blood flow response to a brief tetanic contraction in which potassium (K + ) was infused intra-arterially to elevate the [K + ] o and clamp the smooth muscle membrane potential within the skeletal muscle vascular bed. In six anaesthetized beagle dogs
control contractions increased hindlimb blood flow by 97 ± 14 ml min â1 . During K + infusion the hyperaemic response to contraction was 8 ± 3 ml min â1 . Since the hindlimb blood flow was reduced during K + infusion, a similar reduction in baseline blood flow was produced with phenylephrine infusion. During phenylephrine infusion
the hyperaemic response to contraction was preserved (89 ± 23 ml min â1 ). Recovery contractions performed after the discontinuation of the K + infusion elicited blood flow responses similar to control (100 ± 11 ml min â1 ). In a separate experimental protocol using the isolated gastrocnemius muscle of mongrel dogs ( n = 6) K + infusion did not alter force production by the skeletal muscle. Our data indicate that in the absence of vasodilatation,
there is virtually no change in blood flow. One implication of this finding is that the muscle pump cannot be responsible
for the initial contraction-induced hyperaemia. We conclude that the increase in blood flow immediately following a single
muscle contraction is due to vasodilatation, presumably as a consequence of smooth muscle hyperpolarization.</abstract><cop>9600 Garsington Road , Oxford , OX4 2DQ , UK</cop><pub>The Physiological Society</pub><pmid>15073277</pmid><doi>10.1113/jphysiol.2004.062836</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Blood Pressure - physiology Cell Polarity - physiology Dogs Electrophysiology Female Hindlimb - blood supply Hyperemia - physiopathology In Vitro Techniques Male Muscle Contraction - physiology Muscle, Skeletal - blood supply Muscle, Skeletal - physiopathology Potassium - pharmacology Regional Blood Flow - physiology Research Papers Vasodilation - physiology |
title | Vasodilatation is obligatory for contraction-induced hyperaemia in canine skeletal muscle |
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