The present study investigated the effect of one bout of moderate-intensity exercise on the adrenergic receptor-dependent and -independent vasoconstrictor response in rat aortas, and the role of nitric oxide (NO) bioavailability on these vasomotor responses. One group of rats was submitted to a 60 min of exercise at approximately 60% of maximal exercise capacity on a treadmill (exercise group) and the other one was placed in the treadmill without running (control group). Immediately after this period, both groups were euthanized and the thoracic aorta was removed to evaluate the vasoconstrictor response to norepinephrine and potassium chloride, and to evaluate the vascular nitrite and nitrate concentration. One bout of exercise attenuated the maximal contractile response to both norepinephrine and potassium chloride compared to control group. These differences on vascular reactivity were not observed in endothelium-denuded aortic rings and aortic rings pre-incubated with a nitric oxide synthesis inhibitor. Additionally, exercise group increased NO bioavailability (nitrite and nitrate concentration) as compared to control group. These results demonstrate that one bout of moderate-intensity exercise is able to attenuate adrenergic receptor-dependent and -independent vasoconstrictor response in rat aorta, mainly by increasing vascular NO bioavailability.

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We recorded and analyzed electrogastrograms (EGGs) from 12 patients following distal gastrectomy. The EGGs were recorded from between 3 and 262 months post-operatively. Gastric electrical activity, which showed a distinct repeating pattern with a frequency of 3 cycles per minute (cpm), was easily recognizable in subjects who were recorded 16-20 years postoperatively, but was not clearly evident in EGG running spectra of subjects with a shorter postoperative period. Although the postprandial instability factor of the 3-cpm components (standard deviation of mean spectral frequency of peak 3-cpm group/mean of the 3-cpm spectral frequency) of the epigastric and supraumbilical EGGs showed a significant negative linear correlation with postoperative months, no such correlation was seen in the postprandial to fasting power ratio (postprandial power / fasting power) of the 3-cpm activity component. Therefore, we hypothesized that the disorganized pacemaker activity of the remnant stomach following distal gastrectomy can be reorganized to work as a synchronized unit over a long postoperative recovery period of from 15 to 20 years. A greater degree of epigastric and supraumbilical fasting 6-cpm power seemed to result in a worse quality of life (QOL). Similarly, a larger ratio of the supraumbilical postprandial to fasting power ratio of the 6-cpm activity seemed to result in a worse QOL. In contrast a larger ratio of the infaraumbilical postprandial to fasting power content of the 6-cpm activity seemed to result in a better QOL.

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Statins have been proposed as a novel treatment of respiratory diseases. To determine the beneficial effects of statins on the airway hyperresponsiveness, a characteristic feature of allergic bronchial asthma, the effect of systemic treatment with lovastatin on antigen-induced bronchial smooth muscle hyperresponsiveness was investigated in mice. Male BALB/c mice were sensitized and repeatedly challenged with ovalbumin antigen. Animals were also treated with lovastatin (4 mg/kg/day, i.p.) once a day prior to and during the antigen inhalation period. The bronchial smooth muscle responsiveness to acetylcholine, but not to high K⁺-depolarization, was markedly and significantly augmented in the repeatedly antigen challenged mice. The bronchial smooth muscle hyperresponsiveness to acetylcholine induced by antigen exposure was significantly attenuated by the systemic treatment with lovastatin. Thus, lovastatin might have therapeutic potential to ameliorate airway hyperresponsiveness in allergic bronchial asthma.

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The present study evaluated the effects of histamine 10^-2 M on longitudinal preparations of rat portal vein. It was observed that histamine 10^-2 M induced relaxation of rat portal vein preparations pre-contracted with phenylephrine 10^-4 M. On the other hand, no pharmacological effects were observed in preparations not pre-contracted. The observed histamine-induced relaxing effect was absent in preparations pre-contracted with KCl (120 mM) or in the presence of depolarizing nutritive solution. However, the histamine-induced relaxation was still present in the endothelium-removed preparations. The histamine-induced relaxation also was not prevented by astemizole (10^-6 M, 10^-5 M and 10^-4 M), cimetidine (10^-5 M, 10^-4 M and 10^-3 M) or thioperamide (10^-6 M, 10^-5 M and 10^-4 M), selective antagonists H₁, H₂ and H₃, respectively. The presence of L-NAME 10^-4 M or L-NAME 10^-4 M plus indomethacin 10^-5 M also did not prevent the histamine-induced relaxation observed in rat portal vein. Thus, the histamine-induced relaxation observed in rat portal vein appears to involve a non-endothelial hyperpolarizing mechanism independent of H₁, H₂ and H₃ receptors.

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This study was prompted by the inconsistent reports and apparent controversies that exist in the biomedical literature on the responses of diabetic bladder strips to cholinergic nerve stimulation or exogenously-administered muscarinic agonists, especially acetylcholine (ACh). In the present study, acetylcholine-induced contractions of urinary bladders isolated from normoglycaemic (normal) and streptozotocin-treated, diabetic Wistar rats were examined under physiological conditions. Mechanical contractile changes of the isolated urinary bladders of STZ-treated, diabetic rats in response to bath-applied acetylcholine were compared with those obtained from isolated urinary bladders of normal, age-matched, control rats. Results obtained show that urinary bladders from diabetic rats were always more spontaneously active after mounting, than those of the age-matched normal, control rats. ACh (10^-8-10 ^-4 M) provoked concentration-related, atropine-sensitive contractions of the isolated urinary bladders of both diabetic and age-matched normal, control rats. However, acetylcholine always induced more powerful and greater contractions of the diabetic bladders compared with bladders from the age-matched normal, control rats. The magnitude and/or intensity of the diabetic bladder enhanced contractile responses to ACh continued to increase as the diabetic state of the animals progressed.

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