Biomedical subjects
Publications and source records attributed to K Tazumi.
A 86-year-old woman was admitted to our hospital following vomiting of a small amount of blood. On the 8th hospital day, the patient suddenly died of massive hematemesis. Autopsy disclosed thoracic aortic aneurysm with esophageal fistula.
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1. Serum dopamine beta-hydroxylase activity was determined in normotensive control subjects and patients with labile or established essential hypertension. The enzyme activity was 25-9 +/- 1-9 (SEM) 29-6 +/- 2-5 and 25-1 +/- 1-9 micronmol min-1 1-1, for control, labile and established hypertensive subjects respectively. 2. Neither blood pressure nor serum dopamine beta-hydroxylase activity was changed in normotensive control subjects by administration of phentolamine; however, in patients with essential hypertension blood pressure was significantly decreased (P is less than 0-01) and serum dopamine beta-hydroxylase activity was slightly increased. With propranolol administration, blood pressure and the serum enzyme activity were not significantly changed in normotensive or hypertensive subjects. 3. Our results suggest that there is no correlation between serum dopamine beta-hydroxylase activity and blood pressure.
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The Ca2+ antagonistic coronary vasodilator, Nifedipine, was sublingually administered by a dose of 30 mg to 19 patients with hypertension. Blood pressure of patients with with essential hypertension (n=14) decreased from 177 +/- 24 to 123 +/- 13 mmHg systolic and from 108 +/- 12 to 80 +/- 11 mmHg diastolic (mean +/- SD) (p less than 0.01). Plasma renin activity (PRA) increased significantly from 0.73 +/- 0.62 to 1.50 +/- 1.02 ng/ml/h (p less than 0.05). The same tendency was observed in malignant and renovascular hypertension. In primary aldosteronism (n = 2), blood pressure decreased but PRA did not increase. Hypotensive action and increased plasma renin activity by Ca2+ antagonist, Nifedipine, were clearly demonstrated in patients with hypertension.
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Elevated serum DBH (dopamine-beta-hydroxylase) activity was found in essential hypertension. The elevated level was not reduced when blood pressure was brought to normotensive level by administration of thiazide or rauwolfia. In contrast, serum DBH activity was low in both normotensive and hypertensive patients treated on prolonged hemodialysis. However, there was no correlation between serum DBH activity and blood pressure level. It was suggested that the pathogenesis of high blood pressure might be different between essential hypertension and hypertension with chronic renal failure, and that measurement of serum DBH activity might help for clinical differentiation of essential hypertension from certain forms of secondary hypertension.
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