Answers are grounded in this paper and cite their sources.
The study demonstrates that cardiac endothelin-1 production is upregulated in response to pressure overload but not volume overload in a rat model of hypertrophy.
Although endothelin-1 (ET-1) has been shown to have potent hypertrophic effects in cultured cardiac myocytes, there is no evidence that the production of ET-1 is altered in the hypertrophied heart in vivo. We investigated mRNA and peptide levels of ET-1 in the rat heart hypertrophied due to pressure or volume overload. One week after surgery of abdominal aortic banding (AB) or aortic valve regurgitation (AR; the aortic valve was destroyed by a polyethylene catheter), the rats were sacrificed. Control sham-operated rats were also studied (AB-sham and AR-sham). The left ventricular (LV) weight to body weight ratio was significantly higher in AB rats than in AB-sham rats. It was also significantly higher in AR rats than in AR-sham rats. Therefore, AB rats and AR rats developed LV hypertrophy due to pressure and volume overload, respectively. The expression of ET-1 mRNA in the LV was markedly higher in AB rats than in AB-sham rats. The peptide level of ET-1 was also significantly higher in the LV of AB rats than in that of AB-sham rats. However, the expression of ET-1 mRNA in the LV of AR rats was similar to that of AR-sham rats. The present findings suggest that the production of ET-1 in the heart differs between pressure and volume overload-induced hypertrophy in rats.
No takes yet. Share an insight, caveat, or question.
Sakai et al. (1995) studied Left ventricular hypertrophy. Abdominal aortic banding (AB) or aortic valve regurgitation (AR) vs. Sham-operated rats was evaluated on Expression of ET-1 mRNA and peptide levels in the left ventricle.
Synapse has enriched 10 related papers. Consider them for comparative context: