Key result
β-adrenergic receptor activation with isoproterenol failed to consistently improve myocardial relaxation or reduce LV filling pressures in rat models of hypertensive heart disease.
Why the study?
Does β-adrenergic receptor activation improve left ventricular diastolic function and filling pressures in rat models of hypertensive heart disease?
Does β-adrenergic receptor activation improve left ventricular diastolic function and filling pressures in rat models of hypertensive heart disease?
Beta-adrenergic receptor activation may fail to improve myocardial relaxation and reduce LV filling pressures in hypertensive heart disease with diastolic dysfunction.
Does not support β-adrenergic activation to enhance relaxation in hypertensive heart disease; leaves open human translation.
BACKGROUND: Hypertension is a major cause of left ventricular (LV) diastolic dysfunction. Although β-adrenergic receptor (β-AR) blockers are often used to manage hypertension, the impact of β-AR activation on LV lusitropic effects and hence filling pressures in the hypertensive heart with LV diastolic dysfunction is uncertain. METHODS: Using tissue Doppler imaging and Speckle tracking software, we assessed LV function in isoflurane anesthetised spontaneously hypertensive (SHR) and Dahl salt-sensitive (DSS) rats before and after β-AR activation [isoproterenol (ISO) administration]. RESULTS: As compared to normotensive Wistar Kyoto control rats, or DSS rats not receiving NaCl in the drinking water, SHR and DSS rats receiving NaCl in the drinking water had a reduced myocardial relaxation as indexed by lateral wall e' (early diastolic tissue velocity at the level of the mitral annulus) and an increased LV filling pressure as indexed by E/e'. However, LV ejection fraction and deformation and motion were preserved in both SHR and DSS rats. The administration of ISO resulted in a marked increase in ejection fraction and decrease in LV filling volumes in all groups, and an increase in e' in SHR, but not DSS rats. However, after ISO administration, although E/e' decreased in DSS rats in association with a reduced filling volume, E/e' in SHR remained unchanged and SHR retained greater values than Wistar Kyoto control. CONCLUSIONS: The hypertensive heart is characterized by reductions in myocardial relaxation and increases in filling pressures, but β-AR activation may fail to improve myocardial relaxation and when this occurs, it does not reduce LV filling pressures.
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Bamaiyi et al. (2018) studied Hypertensive Heart Disease with LV diastolic dysfunction. β-AR activation (isoproterenol administration) vs. Baseline (before administration) and normotensive controls was evaluated on LV function (myocardial relaxation indexed by lateral wall e' and LV filling pressure indexed by E/e'). β-adrenergic receptor activation with isoproterenol failed to consistently improve myocardial relaxation or reduce LV filling pressures in rat models of hypertensive heart disease.
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