The cardiovascular integration center not only sends out signals to offset the stimulus-induced responses but also resets the resting blood pressure. We hypothesize that GABAergic adaptations in the hypothalamus participate in the chronic exercise-induced cardiovascular resetting effects in conscious normotensive animals.Male Wistar rats were subjected to chronic moderate exercise (CME, 8-week treadmill running at moderate intensity). A biotelemetry system was used to measure blood pressure, heart rate, autonomic nervous activities, baroreflex sensitivity and endogenous GABAergic activities in the paraventricular nucleus and the posterior hypothalamic area. Hypothalamic specimens were collected for quantifying GABA-related proteins and GABAergic neurons.CME reduced resting blood pressure, heart rate, sympathetic activity and enhanced parasympathetic activity and baroreflex sensitivity. Additionally, CME elevated the resting level of hypothalamic GABAergic activities, increased the percentage of GABAergic neurons in the hypothalamus and upregulated the hypothalamic protein levels of neuronal nitric oxide synthase, GAD67 and gephyrin, but not GABAA receptor. Moreover, a single bout of moderate exercise transiently elevated blood pressure and heart rate with prolonged high levels of neural controls (sympathetic activity, baroreflex sensitivity and hypothalamic GABAergic activities). CME accelerated the postexercise recovery in cardiovascular parameters and neural control alterations.Chronic treadmill running in normotensive rats augmented the GABAergic system in both paraventricular nucleus and posterior hypothalamic area, resulting in lower resting blood pressure, heart rate and sympathetic tone under conscious unrestraint conditions. This study provides insight into mechanisms important for explaining how chronic exercise resets the resting blood pressure.
Summary Thrombolytic therapy is known to induce platelet-related side effects. We used a parallel-plate flow chamber, which was connected to the femoral artery of the rat, to measure platelet adhesion ex vivo. A collagen-coated arterioarterial shunt between two carotid arteries was used to measure shunt patency duration as an index of antithrombotic efficacy. Tissue-type plasminogen activator (t-PA), vitamin E, and the combination of these two were intravenously administered for 60 min. Measurements were performed before drug administration, and at 30, 60, 120 min after the initiation of drug infusion. Our results indicated that (1) treatments with t-PA or t-PA/vitamin E prolonged the time to shunt occlusion at 30 and 60 min; (2) t-PA enhanced platelet adhesion at 60 and 120 min; (3) vitamin E tended to reduce platelet adhesion; (4) t-PA/vitamin E reduced the t-PA-enhanced platelet adhesion; (5) at the high-density area of platelet adhesion under t-PA treatment, the adherent platelets demonstrated severe morphological changes which could be blocked by vitamin E. These data suggest that t-PA may enhance platelet adhesion in rats and that this adverse effect can be suppressed by co-administration of vitamin E.
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