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We had a patient with sleep apnea syndrome, whose circadian variation of blood pressure showed an unusual pattern that systolic blood pressure was higher in the nighttime (22:00-06:00) rather than the daytime (06:00-22:00). With bilateral tonsillectomy and weight reduction, he was much improved from sleepp apnea syndrome, and arterial oxygen tension increased from 65.0mmHg to 83.3mmHg. His circadian variation of blood pressure was also normalized and the heart rate in the nighttime was much lowered. Thus, an unusual circadian variation of blood pressure observed seemed to be associated with sympathetic activation triggered by hypoxia., 論文

To clarify whether or not sodium restriction has an influence on central mechanisms of hypertension, we investigated characteristics of $ \alpha $1-and $ \alpha $2-adrenoceptors in central nervous system in SHR fed on low sodium diet. SHR and wistar-Kyoto rats (WKY) were divided into 2 groups and fed on either low sodium diet containing 0.05% sodium or normal sodium diet containing 0.4% sodium from 3 weeks of age. The experiments were performed at 6,8 and 20 weeks of age. The rat brains were divided into cortex, hypothalamus and lower brainstem. Plasma membranes were prepared, and radioligand binding studies were performed using [^3H]prazosin for $ \alpha $1-adrenoceptors and [^3H]rauwolscine for $ \alpha $2-adrenoceptors. There was no difference in body wight between low and normal sodium diet, while WKY remained normotensive. The Bmax of $ \alpha $1-adrenoceptor was increased significantly in the cortex and hypothalamus in SHR fed on normal sodium diet at 20 weeks of age and in the cortex, hypothalamus, and lower brainstem in SHR fed on low sodium diet at 8 weeks of age compared with those of respective WKY. There was no consistent change in Kd of $ \alpha $1-adrenoceptor in SHR compared with WKY. The Bmax of $ \alpha $2-adrenoceptor was increased in the cortex and hypothalamus in SHR fed on normal sodium diet at 8 weeks of age compared with WKY on the same diet and at the same age, while no increase in SHR fed on low sodium diet was observed. The Kd of $ \alpha $2-adrenoceptor was not changed consistently in SHR on either sodium diet. These results suggest that an increase in $ \alpha $1-adrenoceptor Bmax in hypothalamus might be related genetically to the initiation of hypertension in SHR.

To clarify whether or not sodium restriction has an influence on central mechanisms of hypertension, we investigated characteristics of $ \alpha $1-and $ \alpha $2-adrenoceptors in central nervous system in SHR fed on low sodium diet. SHR and wistar-Kyoto rats (WKY) were divided into 2 groups and fed on either low sodium diet containing 0.05% sodium or normal sodium diet containing 0.4% sodium from 3 weeks of age. The experiments were performed at 6,8 and 20 weeks of age. The rat brains were divided into cortex, hypothalamus and lower brainstem. Plasma membranes were prepared, and radioligand binding studies were performed using [^3H]prazosin for $ \alpha $1-adrenoceptors and [^3H]rauwolscine for $ \alpha $2-adrenoceptors. There was no difference in body wight between low and normal sodium diet, while WKY remained normotensive. The Bmax of $ \alpha $1-adrenoceptor was increased significantly in the cortex and hypothalamus in SHR fed on normal sodium diet at 20 weeks of age and in the cortex, hypothalamus, and lower brainstem in SHR fed on low sodium diet at 8 weeks of age compared with those of respective WKY. There was no consistent change in Kd of $ \alpha $1-adrenoceptor in SHR compared with WKY. The Bmax of $ \alpha $2-adrenoceptor was increased in the cortex and hypothalamus in SHR fed on normal sodium diet at 8 weeks of age compared with WKY on the same diet and at the same age, while no increase in SHR fed on low sodium diet was observed. The Kd of $ \alpha $2-adrenoceptor was not changed consistently in SHR on either sodium diet. These results suggest that an increase in $ \alpha $1-adrenoceptor Bmax in hypothalamus might be related genetically to the initiation of hypertension in SHR., 論文

The patient was a 54-year-old man who complained at first transient paralysis of the left hand. He was diagnosed transient ischemic attack(TIA) after close examinations. And then he received ticlopidine, but six months later he suffered from painless myocardial infarction(MI). It was generally accepted that ticlopidine was effective for prevention of stroke after TIA. This agent suppresses platelet aggregation, and so it was expected to be also effective for prevention of MI after TIA. But ticlopidine was not effective for prevention of MI after TIA in this case., 論文

The patient was a 54-year-old man who complained at first transient paralysis of the left hand. He was diagnosed transient ischemic attack(TIA) after close examinations. And then he received ticlopidine, but six months later he suffered from painless myocardial infarction(MI). It was generally accepted that ticlopidine was effective for prevention of stroke after TIA. This agent suppresses platelet aggregation, and so it was expected to be also effective for prevention of MI after TIA. But ticlopidine was not effective for prevention of MI after TIA in this case.