Beschreibung:
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<jats:list-item><jats:p>In rats a single injection of the alkaloid monocrotaline (60 mg MCT kg<jats:sup>−1</jats:sup> body weight, i.p.) caused right ventricular hypertrophy and heart failure. The aim of this study was to find out whether, in these MCT‐treated rats, the cardiac neuronal noradrenaline uptake (uptake<jats:sub>1</jats:sub>) might undergo chamber‐specific alterations.</jats:p></jats:list-item>
<jats:list-item><jats:p>For this purpose we assessed in right and left ventricular slices, uptake<jats:sub>1</jats:sub> activity (by [<jats:sup>3</jats:sup>H]‐noradrenaline accumulation), and in right and left ventricular membranes, uptake<jats:sub>1</jats:sub> carrier protein density (by [<jats:sup>3</jats:sup>H]‐nisoxetine binding).</jats:p></jats:list-item>
<jats:list-item><jats:p>Uptake<jats:sub>1</jats:sub>‐inhibitors blocked [<jats:sup>3</jats:sup>H]‐noradrenaline accumulation in ventricular slices and [<jats:sup>3</jats:sup>H]‐nisoxetine binding in ventricular membranes with the order of potency: desipramine>nisoxetine>>cocaineGBR 12909, indicating that with both approaches noradrenaline uptake<jats:sub>1</jats:sub> was determined.</jats:p></jats:list-item>
<jats:list-item><jats:p>In right ventricular slices of MCT‐treated rats uptake<jats:sub>1</jats:sub> activity was significantly lower than in control rats (84.7±8.2 vs 145.1±6.2 pmol noradrenaline mg<jats:sup>−1</jats:sup> tissue 15 min<jats:sup>−1</jats:sup>; <jats:italic>P</jats:italic><0.05). This was accompanied by a significant decrease in the density of [<jats:sup>3</jats:sup>H]‐nisoxetine binding sites (73.7±14.4 vs 125.9±9.1 fmol mg<jats:sup>−1</jats:sup> protein; <jats:italic>P</jats:italic><0.05).</jats:p></jats:list-item>
<jats:list-item><jats:p>In left ventricular slices of MCT‐treated rats uptake<jats:sub>1</jats:sub> activity was not significantly altered (131.2±10.5 vs 116.1±5.2 pmol noradrenaline mg<jats:sup>−1</jats:sup> tissue 15 min<jats:sup>−1</jats:sup>); similarly, also the density of [<jats:sup>3</jats:sup>H]‐nisoxetine binding sites was unchanged (108±9.7 vs 123±7.7 fmol mg<jats:sup>−1</jats:sup> protein).</jats:p></jats:list-item>
<jats:list-item><jats:p>We conclude that in MCT‐treated rats with right ventricular hypertrophy and heart failure uptake<jats:sub>1</jats:sub> activity is chamber‐specifically reduced possibly due to a decrease in carrier protein density.</jats:p></jats:list-item>
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</jats:p><jats:p><jats:italic>British Journal of Pharmacology</jats:italic> (2000) <jats:bold>131</jats:bold>, 1438–1444; doi:<jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" xlink:href="10.1038/sj.bjp.0703698">10.1038/sj.bjp.0703698</jats:ext-link></jats:p>