Cardiac infarcts increase sodium transporter transcripts (rBSC1) in the thick ascending limb of Henle

Background. Enhanced expression of the kidney-specific sodium transporter, rBSC1, in the thick ascending limb of Henle (TAL) and of the renal water ch annel, aquaporin-2 (AQP2), in collecting duct has been identified in rats w ith congestive heart failure (CHF) as a cause for enhanced sodium and water retention in this condition. However, the mechanism of impaired urinary so dium excretion observed even in rats with mild cardiac dysfunction remains unknown. Methods. Male Sprague-Dawley rats with myocardial infarctions measuring 15 to 30% of the left ventricular circumference with no overt CHF were prepare d. We measured the amount of rBSC1 or AQP2 mRNA using competitive polymeras e chain reaction (PCR) by inducing a point mutation at the middle of the PC R product for rBSC1 or by deleting 180 bp from the 760 bp PCR product for A QP2, respectively. The results were confirmed by in situ hybridization. rBS C1 protein expression was examined by immunohistochemistry and Western blot analysis using a specific antibody against rBSC1. Results. Although plasma renin activity was slightly elevated in rats with myocardial infarction (MI), no significant differences in lung weight or pl asma concentrations for aldosterone and atrial natriuretic peptide were obs erved between control rats and MI rats. Competitive PCR showed a significan t increase in rBSC1 mRNA in the renal outer medulla and cortex of MI rats, which was confirmed by in situ hybridization. However, the AQP2 mRNA of the se rats remained unchanged throughout the kidney. Renin-angiotensin II bloc kade by oral captopril administration did not influence the alteration in r BSC1 mRNA induced by myocardial infarction. Immunohistochemistry and Wester n blots showed the enhanced expression of rBSC1 protein in TAL of rats with small to moderate cardiac infarcts. Conclusions. rBSC1 is up-regulated even in rats with small to moderate myoc ardial infarctions, which may enhance the sodium transport in the TAL in th is pathophysiologic condition.