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Cardiac infarcts increase sodium transporter transcripts (rBSC1) in the thick ascending limb of Henle
S Nogae1, M Michimata, M Kanazawa
1The Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Insights
Even mild heart dysfunction upregulates the kidney sodium transporter rBSC1 in rats. This enhanced rBSC1 expression in the thick ascending limb may contribute to sodium retention in early cardiac disease.
Area of Science:
- Nephrology
- Cardiology
- Physiology
Background:
- Congestive heart failure (CHF) is linked to sodium and water retention.
- Enhanced kidney sodium transporter (rBSC1) and water channel (AQP2) expression are implicated in CHF.
- Mechanisms of impaired sodium excretion in mild cardiac dysfunction are unclear.
Purpose of the Study:
- Investigate the role of rBSC1 and AQP2 in early-stage cardiac dysfunction.
- Determine the impact of myocardial infarction on renal sodium and water transport mechanisms.
Main Methods:
- Used Sprague-Dawley rats with induced myocardial infarctions (MI).
- Quantified rBSC1 and AQP2 mRNA via competitive PCR and in situ hybridization.
- Assessed rBSC1 protein levels using immunohistochemistry and Western blot.
Main Results:
- MI rats showed increased rBSC1 mRNA and protein in the renal outer medulla and cortex.
- AQP2 mRNA levels remained unchanged in MI rats.
- Renin-angiotensin II blockade did not affect rBSC1 mRNA alterations.
Conclusions:
- rBSC1 is upregulated in rats with small to moderate myocardial infarctions.
- This upregulation may enhance sodium transport in the thick ascending limb.
- rBSC1 may play a role in sodium retention during early cardiac dysfunction.
Background:
Enhanced expression of the kidney-specific sodium transporter, rBSC1, in the thick ascending limb of Henle (TAL) and of the renal water channel, aquaporin-2 (AQP2), in collecting duct has been identified in rats with congestive heart failure (CHF) as a cause for enhanced sodium and water retention in this condition. However, the mechanism of impaired urinary sodium 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 prepared. We measured the amount of rBSC1 or AQP2 mRNA using competitive polymerase chain reaction (PCR) by inducing a point mutation at the middle of the PCR product for rBSC1 or by deleting 180 bp from the 760 bp PCR product for AQP2, respectively. The results were confirmed by in situ hybridization. rBSC1 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 plasma concentrations for aldosterone and atrial natriuretic peptide were observed between control rats and MI rats. Competitive PCR showed a significant 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 these rats remained unchanged throughout the kidney. Renin-angiotensin II blockade by oral captopril administration did not influence the alteration in rBSC1 mRNA induced by myocardial infarction. Immunohistochemistry and Western 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 myocardial infarctions, which may enhance the sodium transport in the TAL in this pathophysiologic condition.