Key result
Experimental supravalvular aortic stenosis in rats increased renal renin gene expression twofold, whereas endothelin and NO synthase gene expression were unchanged.
Why the study?
Does experimental supravalvular aortic stenosis alter renal renin, angiotensin receptor, endothelin, and NOS gene expression in rats?
Does experimental supravalvular aortic stenosis alter renal renin, angiotensin receptor, endothelin, and NOS gene expression in rats?
Effect estimate: Twofold increase in renin gene expression
Experimental supravalvular aortic stenosis in rats stimulates renal renin gene expression without upregulating endothelins or NO synthases, unlike severe heart failure.
Renal renin stimulation in experimental aortic stenosis warrants no clinical action; leaves open human relevance and mechanisms.
BACKGROUND/AIMS: Published data regarding the effects of common cardiovascular diseases, i.e. aortic stenosis on renal regulation of major vasoconstrictive (renin, endothelins) and vasodilatory systems (NO) are controversial. Therefore we aimed to evaluate the effects of chronic aortic stenosis on the renal renin-angiotensin, endothelin and NO systems. METHODS: Experimental supravalvular aortic stenosis was induced by using silver clips with a 0.6 mm internal diameter on the ascending aorta of weanling rats. Renal endothelin-1 (ET-1), endothelin-3 (ET-3), renin, AT(1a), AT(1b), eNOS, and bNOS gene expression were assessed by RNase protection assay. RESULTS: Renal renin gene expression increased twofold in rats with aortic stenosis. In contrast, renal ET-1, ET-3, eNOS, bNOS, and AT(1a), AT(1b) gene expression were unchanged in rats with aortic stenosis. CONCLUSION: Our study demonstrates that in rats with severe experimental supravalvular aortic stenosis only renal renin gene expression is stimulated. This contrasts with severe heart failure where endothelins and NO synthases are also upregulated. Different patterns of regulation of renal vasoactive mediators may be of importance for the extent of the renal impairment associated with aortic stenosis, and may be correlated with the severity of congestive heart failure.
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Kammerl et al. (2002) studied Aortic stenosis. Experimental supravalvular aortic stenosis vs. Control (implied) was evaluated on Renal renin, AT(1a), AT(1b), ET-1, ET-3, eNOS, and bNOS gene expression (Twofold increase in renin gene expression). Experimental supravalvular aortic stenosis in rats increased renal renin gene expression twofold, whereas endothelin and NO synthase gene expression were unchanged.
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