Beschreibung:
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<jats:list-item><jats:p>The effect of induction of capacitative Ca<jats:sup>2+</jats:sup> entry (CCE) upon tone in small (i.d. 200–500 μm) intrapulmonary (IPA), mesenteric (MA), renal (RA), femoral (FA), and coronary arteries (CA) of the rat was examined.</jats:p></jats:list-item>
<jats:list-item><jats:p>Following incubation of IPA with 100 n<jats:sc>M</jats:sc> thapsigargin (Thg) in Ca<jats:sup>2+</jats:sup>‐free physiological salt solution (PSS), a sustained contraction was observed upon reintroduction of 1.8 m<jats:sc>M</jats:sc> Ca<jats:sup>2+</jats:sup>, which was unaffected by either diltiazem (10 <jats:italic>μ</jats:italic><jats:sc>M</jats:sc>) or the reverse mode Na<jats:sup>+</jats:sup>/Ca<jats:sup>2+</jats:sup> antiport inhibitor KB‐R7943 (10 <jats:italic>μ</jats:italic><jats:sc>M</jats:sc>). An identical protocol failed to elicit contraction in MA, RA, or CA, while a small transient contraction was sometimes observed in FA.</jats:p></jats:list-item>
<jats:list-item><jats:p>The effect of this protocol on the intracellular Ca<jats:sup>2+</jats:sup> concentration ([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) was assessed using Fura PE3‐loaded IPA, MA, and FA. Reintroduction of Ca<jats:sup>2+</jats:sup> into the bath solution following Thg treatment in Ca<jats:sup>2+</jats:sup>‐free PSS caused a large, rapid, and sustained increase in [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> in all the three types of artery.</jats:p></jats:list-item>
<jats:list-item><jats:p>100 n<jats:sc>M</jats:sc> Thg induced a slowly developing noisy inward current in smooth muscle cells (SMC) isolated from IPA, which was due to an increase in the activity of single channels with a conductance of ∼30 pS. The current had a reversal potential near 0 mV in normal PSS, and persisted when Ca<jats:sup>2+</jats:sup>‐dependent K<jats:sup>+</jats:sup> and Cl<jats:sup>−</jats:sup> currents were blocked; it was greatly inhibited by 1 <jats:italic>μ</jats:italic><jats:sc>M</jats:sc> La<jats:sup>3+</jats:sup>, 1 <jats:italic>μ</jats:italic><jats:sc>M</jats:sc> Gd<jats:sup>3+</jats:sup>, and the IP<jats:sub>3</jats:sub> receptor antagonist 2‐APB (75 <jats:italic>μ</jats:italic><jats:sc>M)</jats:sc>, and by replacement of extracellular cations by NMDG<jats:sup>+</jats:sup>.</jats:p></jats:list-item>
<jats:list-item><jats:p>In conclusion, depletion of intracellular Ca<jats:sup>2+</jats:sup> stores with Thg caused capacitative Ca<jats:sup>2+</jats:sup> entry in rat small muscular IPA, MA, and FA. However, a corresponding contraction was observed only in IPA. CCE in IPA was associated with the development of a small La<jats:sup>3+</jats:sup>‐ and Gd<jats:sup>3+</jats:sup>‐sensitive current, and an increased Mn<jats:sup>2+</jats:sup> quench of Fura PE‐3 fluorescence. These results suggest that although CCE occurs in a number of types of small arteries, its coupling to contraction appears to be of particular importance in pulmonary arteries.</jats:p></jats:list-item>
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</jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (2003) <jats:bold>140</jats:bold>, 97–106. doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0705408">10.1038/sj.bjp.0705408</jats:ext-link></jats:p>