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Evidence for a common mechanism for spontaneous rhythmic contraction and myogenic contraction induced by quick stretch in detrusor smooth muscle
Author(s) -
Komari S. Omid,
Headley Patrick C.,
Klausner Adam P.,
Ratz Paul H.,
Speich John E.
Publication year - 2013
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.1002/phy2.168
Subject(s) - contraction (grammar) , muscle contraction , population , chemistry , biophysics , rhythm , medicine , endocrinology , biology , environmental health
Detrusor smooth muscle exhibits myogenic contraction in response to a quick stretch ( QS ) as well as spontaneous rhythmic contraction ( SRC ); however, whether the same population of actomyosin crossbridges with a common regulatory mechanism is responsible for these two types of contraction has not been determined. Detrusor strips from New Zealand white rabbit bladders were allowed to develop SRC at a reference muscle length ( L ref ), or rhythmic contraction ( RC ) was induced with tetraethylammonium ( TEA ). Multiple 10‐msec stretches of 15% L ref were then imposed at L ref randomly during the rhythm cycle, and the nadir‐to‐peak ( NTP ) tension amplitude of the resulting myogenic contraction was measured. The amplitude and period of the rhythm cycle were measured prior to each QS . NTP was larger when a QS was imposed during a portion the cycle when tension was smaller ( n  = 3 each SRC and TEA ‐induced RC ). These data suggest that when the rhythmic mechanism was mostly inactive and tension was near a minimum, a larger portion of a shared population of crossbridges was available to produce a myogenic response to a QS . Rho kinase, cyclooxygenase‐1, and cyclooxygenase‐2 inhibitors (H‐1152, SC ‐560, and NS ‐398) affected SRC amplitude and NTP amplitude following a QS to the same degree ( n  = 3 each drug), providing additional evidence to support the hypothesis that a common mechanism is responsible for SRC and myogenic contraction due to QS . If a common mechanism exists, then QS is a potential mechanical probe to study SRC regulation and its alteration in overactive bladder.

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