Increased susceptibility to atrial tachyarrhythmia in spontaneously hypertensive rat hearts.

Although hypertension is the most prevalent risk factor for atrial fibrillation, there is currently no information available from animal models of hypertension regarding the development of atrial remodeling or increased susceptibility to atrial tachyarrhythmia. Therefore, we examined the susceptibility to atrial tachyarrhythmia and the development of atrial remodeling in excised perfused hearts from male spontaneously hypertensive rats in comparison with age-matched male Wistar-Kyoto normotensive controls at age 3 and 11 months, corresponding with early hypertension and pre-heart failure stages, respectively. The incidence and duration of left atrial tachyarrhythmia induced by burst pacing was greater in hearts from 11-month-old hypertensive animals than either in age-matched controls or in 3-month-old hypertensive rats, although there was no difference between hypertensive and normotensive hearts at 3 months.

Evidence for a novel K(+) channel modulated by alpha(1A)-adrenoceptors in cardiac myocytes.

Accumulating evidence suggests that steady-state K(+) currents modulate excitability and action potential duration, particularly in cardiac cell types with relatively abbreviated action potential plateau phases. Despite representing potential drug targets, at present these currents and their modulation are comparatively poorly characterized. Therefore, we investigated the effects of phenylephrine [PE; an alpha(1)-adrenoceptor (alpha(1)-AR) agonist] on a sustained outward K(+) current in rat ventricular myocytes.

Gender-related differences in ventricular myocyte repolarization in the guinea pig.

It is well established that gender-differences exist in cardiac electrophysiology and these are thought to contribute to the increased risk of women, compared to men, for the potentially lethal ventricular arrhythmia, torsades de pointes. Data from animal models with abbreviated estrus cycles suggest that androgens may play a protective role in males. However, the role of female sex hormones in gender-differences in cardiac electrophysiology is less clear.