Estrogen exerts many effects on the vascular endothelium. Calmodulin (CaM) is the transducer of Ca 2؉ signals and is a limiting factor in cardiovascular tissues. It is unknown whether and how estrogen modifies endothelial functions via the net-

There was a risk of interactions between a biological CAM method and conventional drugs in 54.9% of the patients using CAM. To raise knowledge on interactions a better training for doctors with respect to CAM is strongly needed. Furthermore, patients' awareness should also be raised and communication between physician and patient on the topic improved.

Exposure to social and environmental stressors may influence behavior as well as autonomic and cardiovascular regulation, potentially leading to depressive disorders and cardiac dysfunction including elevated sympathetic drive, reduced parasympathetic function, and ventricular arrhythmias. The cellular mechanisms that underlie these interactions are not well understood. One mechanism may involve alterations in the expression of Connexin43 (Cx43) and Connexin45 (Cx45), gap junction proteins in the heart that play an important role in ensuring efficient cell-to-cell coupling and the maintenance of cardiac rhythmicity. The present study investigated the hypothesis that long-term social isolation, combined with mild environmental stressors, would produce both depressive behaviors and altered Cx43 and Cx45 expression in the left ventricle of prairie voles – a socially monogamous rodent model. Adult, female prairie voles were exposed to either social isolation (n=22) or control (paired, n=23) conditions (4 weeks), alone or in combination with chronic mild stress (1 week). Social isolation, versus paired control conditions, produced significantly (P < 0.05) increased depressive behaviors in a 5-min forced swim test, and chronic mild stress exacerbated (P < 0.05) these behaviors. Social isolation (alone) reduced (P < 0.05) total Cx43 expression in the left ventricle; whereas chronic mild stress (but not isolation) increased (P < 0.05) total Cx45 expression and reduced (P < 0.05) the Cx43/Cx45 ratio, measured via Western blot analysis. The present findings provide insight into potential cellular mechanisms underlying altered cardiac rhythmicity associated with social and environmental stress in the prairie vole.

Supraventricular arrhythmias are the most prevalent of all arrhythmias, with the elderly being at the greatest risk. Exercise training has been repeatedly shown to reduce supraventricular arrhythmic susceptibility. Connexin 40 (Cx40) is known to be the primary regulator of conduction between atrial cardiomyocytes and alteration of its expression has been associated with atrial arrhythmia development. Recent evidence also suggests that Connexin 43 (Cx43) assists in controlling atrial electrical conduction. We hypothesized that exercise training would reduce atrial arrhythmic susceptibility in young and aged animals and would be accompanied by changes in atrial Cx40 and Cx43 expression and/or phosphorylation. Groups of young and aged F344 rats underwent treadmill exercise training or sedentary handling. Subcutaneous electrocardiographic leads were then implanted following the respective exercise or sedentary protocols. The arrhythmic index (AI) was calculated using a modified scoring system totaling supraventricular arrhythmias during a baseline period (BL), sympathoexcitation (isoproterenol, 150 mg/kg s.c), and psychological stressor (BR). AI was significantly reduced during BL and ISO periods in young exercise animals compared to sedentary counterparts. Western blot analysis showed significantly greater atrial Cx43 expression in aged exercise compared to aged sedentary rats, while there was no significant change in the young animals. Preliminary evidence suggests an opposite pattern observed in atrial Cx40 expression, trending towards increased expression in young exercise compared to young sedentary rats, while showing no changes in aged animals. These preliminary results indicate moderate exercise training may be cardioprotective in a young animal model by reducing supraventricular arrhythmias and increasing atrial Cx40 expression while a similar aged model increases atrial Cx43 expression.

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