To evaluate mechanisms responsible for differences between patients showing a nocturnal fall in blood pressure ("dippers") and those showing no such fall in blood pressure ("nondippers"), we performed 24-hour (h) ambulatory blood pressure monitoring in 25 patients with untreated essential hypertension who were 37-49 years of age (16 men and 9 women). The diagnosis of essential hypertension was based on the patients' history, physical examination, routine laboratory tests, and intravenous pyelography. Blood pressure was measured by sphygmomanometer and by noninvasive ambulatory monitoring for 24 h. Exercise was performed on a supine bicycle ergometer. The initial workload was 50 W and was increased progressively by 25 W at 3-min intervals. Plasma and urinary norepinephrine levels were measured by high-performance liquid chromatography. Dippers were defined as patients with a difference of > 10 mmHg in the systolic BP or > 5 mmHg in the diastolic BP between daytime and nighttime. Eleven patients were dippers and 14 patients were nondippers. There was a positive correlation between the nocturnal fall in blood pressure and the rise in blood pressure during exercise (r = 0.54, p < 0.01), and the increase during exercise was greater in dippers than in nondippers. There was also a significant positive correlation between the urinary norepinephrine level and the fall in blood pressure at night (r = 0.75, p < 0.01). A significant increase in plasma norepinephrine during exercise was found in dippers, as compared with nondippers. These results suggest that in patients with hypertension a nocturnal fall in blood pressure is closely related to the blood-pressure response to exercise, and that the attenuation of sympathetic nervous activity might play an important role in the nocturnal decrease in blood pressure.

These results were strongly indicative that the prompt suppression of the PCA by oral l-ephedrine was not exerted following the drug was absorbed from the gastrointestinal tract. Thus, the result may be from an indirect inhibition of chemical mediator release, possibly through an unidentified stimulation of the nervous system, but not from the inhibition of chemical mediator release by the direct interaction of drug to mast cells and not from the decreased vascular permeability.

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The anticonvulsant effects of Shitei-To and its components on maximal electroshock seizures and chemical convulsions were examined. Shitei-To significantly prolonged the latency to bicuculline (2.0 mg/kg, s.c.)-induced clonic convulsions. Repeated treatment with Shitei-To also significantly prolonged the latency to strychnine (1.5 mg/kg, i.p.)-and pentylenetetrazol (90 mg/kg, i.p.)-induced clonic convulsions. On the other hand, Shitei-To had no effect on maximal electroshock seizures. Of the components of Shitei-To, Shitei had almost the same effect as Shitei-To against the clonic convulsions induced by the three chemical agents tested. These findings suggest that Shitei-To has anticonvulsant effects.

The results strongly suggest that beta2-adrenoceptors locate in the stomach and that their receptor excitement finally may lead to the inhibition of PCA via the stimulation of the central and peripheral nervous systems.