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Biomedical subjects

S Shigetomi

Publications and source records attributed to S Shigetomi.

71 records · Page 4Linked to original sources
PubMed1981

[The effects of dexamethasone and captopril on plasma aldosterone response to exogenous angiotensin II in normal men (author's transl)].

The response of plasma aldosterone to exogenous angiotensin II was evaluated in five normal volunteers on three occasions, once without endogenous ACTH or angiotensin II suppression (control), once with ACTH suppression (dexamethasone) and once with ACTH and angiotensin II suppression (dexamethasone and captopril). Plasma aldosterone concentration (PAC) fell from a control of 6.8 +/- 1.6 (mean +/- SEM) to 4.4 +/- 0.4 ng/dl with dexamethasone (p less than 0.05) and to 1.8 +/- 0.2 ng/dl with dexamethasone and captopril (p less than 0.001). PAC increased dose-dependently upon infusion rates of angiotensin II (0.2, 0.4, 0.8, 1.0, 1.2, 2.5 and 5.0 ng/kg/min) on each occasion, but aldosterone responsiveness to infused angiotensin II (change and percentage from base line levels) was not altered by the suppression of endogenous ACTH secretion with dexamethasone with each incremental infusion of the octapeptide. However, change in PAC caused by angiotensin II in the suppression of ACTH and angiotensin II was greater than that in the control at an infusion rate of 0.2 ng/kg/min (p less than 0.05), 1.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01), and it was also greater than that in the suppression of ACTH at an infusion rate of 0.2 ng/kg/min (p less than 0.05) and 2.5 ng/kg/min (p less than 0.01). These results demonstrate that in normal men, base line aldosterone levels are controlled not only by the renin-angiotensin system, but also, in part, by ACTH. The aldosterone response to angiotensin II, however, does not depend upon endogenous ACTH secretion, an action of angiotensin II on the pituitary to release ACTH. Simultaneous administration of dexamethasone and captopril may be a useful tool to assess the sensitivity of aldosterone production in the adrenal glomerulosa with exogenous angiotensin II since endogenous ACTH and angiotensin II can be suppressed by these medications.

Adult↗
PubMed1981

[The correlation between serum angiotensin I-converting enzyme activity and the renin-angiotensin-aldosterone system in hypertensive patients (author's transl)].

In order to investigate the role and origin of serum angiotensin I-converting enzyme activity (ACEA) in hypertension, the correlation between serum ACEA and the renin-angiotensin-aldosterone system was evaluated in hypertensive patients of whom 36 had essential hypertension, five had hypertension associated with chronic renal failure, three had renovascular hypertension, and one had primary aldosteronism. Serum ACEA was 17.0 +/- 3.3 U (mean +/- sd) in the normotensive control, 20.1 +/- 7.1 U in patients with essential hypertension, 11.6 +/- 3.4 U in patients with chronic renal failure, 31.7 +/- 1.1 U in patients with renovascular hypertension, and 9.7 U in primary aldosteronism in a recumbent state. There was a significant correlation between serum ACEA and plasma renin activity (PRA) (r = 0.615, p less than 0.001, n = 45) and plasma aldosterone concentration (PAC) (r = 0.599, p less than 0.001, n = 34) in a recumbent state. However, there was no significant correlation between serum ACEA and mean blood pressure. Serum ACEA elevated with furosemide and an upright posture significantly correlated with elevation in PRA (r = 0.369, p less than 0.05, n = 32) but did not significantly correlate with elevation in PAC. It is suggested, therefore, that the kidney is the suspected source of the plasma activity of the enzyme and that serum ACEA plays a possible role in the regulations of blood pressure and electrolyte metabolism modulating the renin-angiotensin-aldosterone system.

Adult↗
PubMed1981

[A simple and rapid assay for the determination of plasma, urine and tissue catecholamine concentrations by high pressure liquid chromatography with fluorescent reaction (author's transl)].

The method of determining catecholamines has been studied, and such sensitive methods as radioenzymatic assay and gas chromatography are used for their measurement, but these techniques are not widespread because of their complexity. In this study, we developed a high pressure liquid chromatographic method with a fluorescent reaction system for the determination of plasma, urine and tissue catecholamine concentration. The eluates from plasma, urine and tissue were chromatographied on a Hitachi #3011C Gel (2.6 x 250mm) and reacted to the mixed solution of 0.1M KH2PO4, 0.2M K2HPO4 and 0.0075% K3Fe(CN)6 (the first solution), followed by the mixture of 0.1% ascorbic acid and 5N NaOH. A stock solution (0.1mg/ml of norepinephrine, 0.1mg/ml of epinephrine and 2.0mg/ml of dopamine) was stored in 0.2N CH3COOH at 4 degrees C, and was diluted at 1/5,000-1/40,000 when needed. Recovery of norephinephrine after extraction was 54.3-58.9% and that of epinephrine was 49.2-55.8%. The accuracy was acceptable and sensitivity was 30-50pg. The mean plasma norepinephrine concentrations (p-NE) were 105.6 +/- 6.8pg/ml in normal subjects and 157.7 +/- 74.5pg/ml in essential hypertensives (EH). The mean epinephrine concentrations (p-E) were 30.8 +/- 16.3pg/ml in normals and 20.0 +/- 11.9pg/ml in EH. PNE increased after standing or after furosemide plus 2-hour standing, but p-E did not increase as much as p-NE. Catecholamine concentration in the rat brain and adrenal medullary tissue could be determined by the use of this method.

Animals↗
PubMed1981

Methacholine, a cholinergic agent, stimulates catecholamine release in man.

To study the effect of cholinergic stimulation on catecholamine release, methacholine, a choline ester, was injected im into normal subjects. Significant increases in plasma norepinephrine and plasma epinephrine concentrations were observed in response to methacholine administration with significant haemodynamic changes, but there was no correlation between the rise in plasma catecholamines and the haemodynamic changes. These results suggest that the increases in plasma catecholamines induced by methacholine did not result from reflex responses to haemodynamic changes and thus could be a direct effect of methacholine on sympathetic nerves and the adrenal medulla.

Adult↗
PubMed1981

Effect of sodium intake on the brain and the aortic angiotensin-converting enzyme activity in spontaneously hypertensive rat.

Effect of sodium intake on angiotensin-converting enzyme activity was studied in five areas of the brain (cerebral cortex, midbrain, striatum, thalamus and hypothalamus) and in subcellular fractions of the aorta (homogenate, mitochondria, microsomes and supernatant) in normotensive, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats. Angiotensin-converting enzyme activity was significantly higher in the hypothalamic area than in the other areas of the brain in spontaneously hypertensive rat. The enzyme activity of subcellular fractions of the aorta showed an extremely high value in the supernatant in normotensive, spontaneously hypertensive, and stroke-prone spontaneously hypertensive rats. Sodium intake resulted in a marked decrease in the aortic converting enzyme activity, while it did in a significant rise of the enzyme activity in the midbrain area in spontaneously hypertensive rat, and in the midbrain and striatum areas in stroke-prone spontaneously hypertensive rat. It is likely therefore that sodium intake lowers the converting enzyme activity of the aorta. Increased converting enzyme activity of the brain in spontaneously hypertensive rats may play a possible role in hypertension induced by sodium intake.

Animals↗
PubMed1981

[Determination of plasma catecholamine as a quantitative index for the evaluation of sympathetic nervous system function in man during methacholine test (author's transl)].

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.

Adult↗
PubMed1980

[Studies on the blood pressure control mechanism in essential hypertension: the relation of plasma norepinephrine concentrations to plasma renin activity and haemodynamics (author's transl)].

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.

Blood Pressure↗