LIPOPOLYSACCHARIDE-INDUCED REDISTRIBUTION OF MYOCARDIAL CONNEXIN43 IS ASSOCIATED WITH INCREASED MACROPHAGE INFILTRATION IN BOTH NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS

We investigated whether changes in gap junction alpha-1 protein (Cx43) expression may be associated with macrophage-induced inflammation in the heart of spontaneously hypertensive rats (SHR). To examine mutual interactions of macrophage infiltration with Cx43 expression and redistribution, we applied a bolus of bacterial lipopolysaccharide (LPS) to SHR and age-matched normotensive Wistar rats. The results demonstrated association of Cx43 downregulation with increased infiltration of cardiac CD-68 macrophages and upregulation of nuclear factor-kappa B (NF kappa B) and tumor necrosis factor-alpha (TNF-alpha) expression in the heart of SHR. LPS application to SHR caused further degradation and redistribution of Cx43 accompanied with extensively increased macrophage infiltration and NF kappa B and TNF-alpha expression. LPS administration to Wistar rats resulted in elevation of cardiac CD-68 macrophages but it did not significantly affect total Cx43 expression. Our results are suggestive of regulation of Cx43 expression with macrophages-related inflammation in the heart of SHR. The data also indicate that SHR can be more sensitive to LPS than are normotensive rats.