Why the study?
Does long-term treatment with ketanserin or candesartan reverse left ventricular hypertrophy in animal models with arterial baroreflex deficiency?
Does long-term treatment with ketanserin or candesartan reverse left ventricular hypertrophy in animal models with arterial baroreflex deficiency?
Targeting arterial baroreflex function with agents like ketanserin or candesartan may be a feasible strategy for reversing left ventricular hypertrophy.
Answers are grounded in this paper and cite their sources.
Supports baroreflex-targeted LVH reversal in animal models; leaves open translation to human hypertension management.
It is well known that the arterial baroreflex (ABR) plays a key role in the regulation of heart rate and stabilization of blood pressure. Currently, it appears that ABR dysfunction is involved in the pathophysiology of cardiovascular disease states. Since the mid‐1990s, a number of studies have been carried out in our laboratory to explore the pathological significance of ABR function in cardiovascular damage. This minireview summarizes our research work on the topic of ABR function and left ventricular hypertrophy (LVH). On the basis of discussion concerning the importance of ABR dysfunction in hypertensive LVH and sinoaortic denervation‐induced LVH, we advance a new strategy for reversal of LVH, that is, restoration of impaired ABR function. We tested this hypothesis in animal models with ABR deficiency. It was found that improvement of impaired ABR function with long‐term treatment of ketanserin or candesartan was accompanied by reversal of LVH. The preliminary results indicate that it is feasible to target ABR for treatment of LVH. Drug Dev. Res. 58:61–64, 2003.
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Miao et al. (2003) studied this question.
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