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1 Campus Berlin-Buch, Max-Delbrueck-Center for Molecular Medicine (MDC), Berlin, Germany; National Heart, Lung and Blood Institute, Bethesda, MD, USA
2 Charite Campus Berlin-Buch, Humboldt-University, Franz-Volhard-Klinik, Berlin, Germany; National Heart, Lung and Blood Institute, Bethesda, MD, USA
3 Campus Berlin-Buch, Max-Delbrueck-Center for Molecular Medicine (MDC), Berlin, Germany
4 Charite Campus Berlin-Buch, Humboldt-University, Franz-Volhard-Klinik, Berlin, Germany
5 Charite Campus Berlin-Buch, Humboldt-University, Franz-Volhard-Klinik, Berlin, Germany; St. Elisabeth Hospital, Halle, Germany
* To whom correspondence should be addressed. E-mail: langenit{at}nhlbi.nih.gov.
Stored cardiac pro-ANP is converted to ANP and released upon stretch from atria into circulation. Corin is a serin protease with pro-ANP converting properties and may be the rate limiting enzyme in ANP release. This study was aimed to clone and sequence corin in the rat, and to analyze corin mRNA expression in heart failure when ANP release upon stretch is blunted. Full length cDNA of rat corin was obtained from atrial RNA by RT-PCR, and sequenced. Tissue distribution as well as regulation of corin mRNA expression in the atria were determined by RT-PCR and RNase protection assy. Heart failure was induced by an infrarenal aortocaval shunt. Stretch was applied to the left atrium in a working heart modus and ANP was measured in the perfusates. The sequence of rat corin cDNA was found to be 93.6% homologous to mouse corin cDNA. Corin mRNA was expressed almost exclusively in the heart with highest concentrations in both atria. The aortocaval shunt led to cardiac hypertrophy and heart failure. Stretch-induced ANP release was blunted in shunt animals (control 1195 ± 197, shunt 639 ± 99 fmol. min-1.g-1, p<0.05). Corin mRNA expression was decreased in both atria in shunt animals (right atrium: control 0.638 ± 0.004, shunt 0.566 ± 0.014 AU, p<0.001; left atrium: control 0.564 ± 0.009, shunt 0.464 ± 0.009 AU, p<0.001). Downregulation of atrial corin mRNA expression may be a novel mechanism for the blunted ANP release in heart failure.
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