[Hyporeninemic hypoaldosteronism--Conn's syndromes].
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Biomedical subjects
Publications and source records attributed to S Fukuchi.
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For many years blood pressure has been only an index among a number of physiological conditions presenting sympathetic nervous systems activities in methacholine test due largely to the lack of specific and practical method for the determination of catecholamine. We found that methacholine induced a significant increase in plasma catecholamines with an alternation in hemodynamic change in the present study by the use of high speed liquid chromatography and automated THI method. The increments in plasma catecholamines were not correlated with apparent decrements in blood pressure. Therefore the increments in plasma catecholamines induced by methacholine were not attributable to reflex responses to hemodynamic changes and rather could be the direct effect of methacholine on sympathetic neuron and adrenal medullae. Besides there was no correlation between the increments in plasma catecholamines and methacholine indices. These data question the suitability of blood pressure as an index for the evaluation of sympathetic nervous system function during methacholine test and suggest that plasma catecholamines might be a proper parameter for the sympathetic nervous activities response to methacholine.
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A simplified radioimmunoassay system for aldosterone secretion rate was developed by using radioiodine-labelled aldosterone and highly specific antiserum to aldosterone. An antibody was produced in rabbits by injecting aldosterone-oxime coupled with bovine gamma-globulin once a month. Aldosterone-oxime was labelled with 125I by using the chloramine T method described by Hunter and Greenwood. 3 ml of a twenty-four-hour urine specimen was used for the radioimmunoassay. Following CH2Cl2 extraction, pH 1 hydrolysis was carried out for twenty-four hours. Separation of the aldosterone extract was achieved by paper chromatography (hexane:benzene:methanol:water = 1:9:5:2.5). The minimum measurable concentration was under 1pg, and adequate intraassay and interassay precision were obtained. Aldosterone secretion rate was 89.6 +/- 25.8 (mean +/- SD)mug/day in normal subjects and was similar in low- and normal-renin essential hypertension. Significant high values (806.4 +/- 65.8mug/day) were obtained in primary aldosteronism and were slightly high in secondary aldosteronism and high-renin essential hypertension. The aldosterone secretion rate correlated positively with plasma aldosterone level (r = 0.731, p < 0.01). Aldosterone secretion rates were obviously higher than plasma levels in primary and idiopathic aldosteronism. From these results, it is concluded that this method is a very useful and reliable one for measuring aldosterone secretion rate and for discriminating primary aldosteronism from low-renin essential hypertension. it is superior in its simplicity, and there is no need to use a liquid scintillation counter.
To elucidate the mechanism of blood pressure control in essential hypertension (EH), plasma norepinephrine concentrations (PNE), plasma renin activity (PRA), cardiac index (CI) and total peripheral resistance (TPR) were determined in normal subjects and those suffering from EH while resting and after standing with furosemide. The results were as follows: 1) PNE were 204 +/- 100 pg/ml (mean +/- S.D.) in normal subjects and 313 +/- 257 pg/ml in EH. PNE in EH were not significantly greater than in normal subjects, but in some patients with EH, PNE were above normal. 2) In both normal subjects and those suffering from EH, PNE and PRA showed a positive correlation (r = 0.45, p less than 0.05; r = 0.52, p less than 0.001; respectively). 3) In low renin EH, the response of PNE to the stimulation of standing with furosemide was significantly greater than in normal renin EH (p less than 0.05). 4) PNE in EH were independent of both TPR and CI. 5) There was a positive relation between PRA and CI (r = 0.44, p less than 0.05), and a slight negative relation between PRA and TPR (r = 0.36, 0.05 less than p less than 0.1). These results suggest that sympathetic nervous hypertonicity may be responsible for the activation of the renin-angiotensin system and that the interaction of both the sympathetic nervous system and the renin-angiotensin system may play an important role in the elevation of blood pressure. In low renin EH, the response of PNE to the stimulation of standing with furosemide may be normal and blood pressure may be controlled by both the sympathetic nervous system and the renin-angiotensin system.
In this study changes in plasma oxytocin levels were determined before and after ejaculation in patients with abnormal spermatogenesis. Plasma oxytocin levels rose significantly after ejaculation (P < 0.001, n = 17). There was no obvious correlation between plasma oxytocin levels and sperm count, sperm motility or the number of abnormal forms. Oxytocin may play a role in the precipitation of ejaculation in males.
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Twenty-one patients with essential hypertension received a constant infusion of angiotensin II and des-aspartyl1-angiotensin II for 45 min on 2 consecutive days during normal sodium intake. Des-aspartyl1-angiotensin II increased mean blood pressure from 127.5+/-17.7 to 142.3+/-18.8 mmHg and plasma aldosterone concentration from 12.1+/-7.8 to 18.8+/-11.4 ng/100 ml. Although plasma aldosterone concentration elevation was positively correlated with pre-infusion levels of plasma renin activity (r=0.862, p less than 0.001), mean blood pressure elevation was inversely correlated with the values of renin activity (r=-0.599, p less than 0.01). In contrast, elevatins of both plasma aldosterone concentration and mean blood pressure were inversely correlated with pre-infusion levels of plasma renin activity in angiotensin II infusion. Des-asparty1-angiotensin II and angiotensin II were equally effective in suppressing renin release. These data demonstrte that des-aspartyl1-angiotensin II rather than angiotensin II plays an important role in aldosterone production in essential hypertension.