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Biomedical subjects

J Matsui

Publications and source records attributed to J Matsui.

At least 91 records · Page 5Linked to original sources
PubMed1983

Arterial renin--partial characterization and its possible role in the pathogenesis of hypertension.

1) Renin-like enzyme of rat aorta was purified by chromatography with DEAE-cellulose and Sephadex G-200. 2) The molecular weight of renin-like enzyme was 124,000 and 72,000 on Sephadex G-200 gel filtration. The isozymes, however, migrated as a single band with molecular weight of 71,000 on SDS/polyacrylamide gel electrophoresis. These isozymes showed the same optimal pH (6.5) and temperature (37 degrees C). 3) Renin-like enzyme showed high activity in the microsomal fraction of the aorta. 4) In one-clip, two-kidney Goldblatt hypertensive rats, the aortic renin concentration increased significantly, but not parallel with the activity in plasma. 5) Renin, widely distributed in subcellular fractions of the aorta, may play a possible role in the local control of vascular tone. It is likely that renin in vascular wall is of local origin.

Animals↗
PubMed1983

Angiotensin-converting enzyme activity of the brain and the aorta in experimental hypertensive rats.

Angiotensin-converting enzyme activity in six areas of the brain (cerebral cortex, midbrain, thalamus, hypothalamus, striatum, and cerebellum) and subcellular fractions of the aorta (homogenate, mitochondria, microsomes, and supernatant) was determined in both normotensive and renal hypertensive rats [Goldblatt one-clip, one-kidney (1-c, 1-k) and one-clip, two-kidney (1-c, 2-k) hypertensive, and two-clip, two-kidney (2-c, 2-k) hypertensive rats]. Converting-enzyme activity was relatively high in the thalamus and relatively low in the cerebellum in normotensive and renal hypertensive rats. The enzyme activity in the hypothalamus of Goldblatt 1-c, 2-k rats was significantly higher than that of normotensive and other renal hypertensive rats. However, there was no significant difference in the enzyme activity in each brain area among normotensive, Goldblatt 1-c, 1-k hypertensive and 2-c, 2-k hypertensive rats. The enzyme activity of the supernatant from aortic subcellular fractions was extremely high in normotensive and renal hypertensive rats. However, the enzyme activity in all aortic fractions from Goldblatt 1-c, 2-k rats was significantly higher than that of normotensive and other renal hypertensive rats. There was no significant difference in the enzyme activity among normotensive, Goldblatt 1-c, 1-k hypertensive and 2-c, 2-k hypertensive rats. Therefore, it is likely that increased angiotensin-converting enzyme activity in the brain and the aorta may play a role in the initiation or the maintenance of hypertension in Goldblatt 1-c, 2-k hypertensive rats.

Animals↗
PubMed1983

Acute effects of captopril on serum angiotensin-converting enzyme activity, the renin-aldosterone system and blood pressure in patients with sarcoidosis.

Captopril, an orally active angiotensin-converting enzyme (ACE) inhibitor, was administered to three patients in an active stage of sarcoidosis. The serum ACE level, aldosterone concentration in plasma and blood pressure decreased rapidly after administration, while plasma renin activity was not significantly changed. It is suggested that inhibition of ACE by captopril offers a possible therapeutic approach to the treatment of sarcoidosis.

Adult↗
PubMed1982

[Angiotensin-converting enzyme activity of the aorta in experimental hypertensive rats].

Angiotensin-converting enzyme activity of the aortic subcellular fractions (homogenate, mitochondria, microsomes and supernatant) was determined in normotensive and experimental hypertensive rats (1-clip, 1-kidney Goldblatt hypertensive; 1-clip, 2-kidney Goldblatt hypertensive and 2-clip, 2-kidney hypertensive rats). The systolic blood pressure markedly elevated in each group of experimental hypertensive rats, while it did not in normotensive rats. Angiotensin-converting enzyme activity was consistently high in the microsomal and supernatant fractions of the aorta in experimental hypertensive rats as well as in normotensive rats. However, the enzyme activity from each fraction of the aorta in 1-clip, 2-kidney Goldblatt hypertensive rats was significantly higher than that in normotensive and other experimental hypertensive rats. There was no significant difference in the enzyme activity among normotensive, 1-clip, 1-kidney Goldblatt hypertensive and 2-clip, 2-kidney hypertensive rats. The angiotensin-converting enzyme, widely distributed in subcellular fractions of the aorta, may play a possible role in the local control of vascular tone. It seems likely that increased angiotensin-converting enzyme activity in arterial tissue contributes to the initiation or development of hypertension in 1-clip, 2-kidney Goldblatt hypertension in rats.

Animals↗
PubMed1982

[Clinical study on the angiotensin I-converting enzyme in human urine. (I) Partial purification, enzymic characteristics and excretion in normal subjects].

The angiotensin I-converting enzyme in normal human urine was partially purified with ammonium surfate (3.2M), DEAE-Cellulose ion exchange chromatography (0-0.5M NaCl gradient), and Sephadex G 200 gel filtration. The enzyme was separated into three forms which had different molecular weights of 700000, 290000 and 40000, respectively. The enzymic biochemical characteristics of these three enzymes, however, were identical with regard to their inhibitory effects (bradykinin potentiator c, arg-pro-pro, o-phenanthroline and EDTA), Cl- dependency, optimal pH (8.3) and temperature (37 degrees C), and Km value (2.3mM). The enzymic activity was determined in five normal subjects in three conditions of dietary sodium intake (51, 153 and 340mEq for 5 days, respectively). The enzymic activity correlated well with the concentration of the excreted sodium (r = 0.87, p less than 0.001). There was no significant relation between the enzymic excretion and the concentration of the excreted potassium, nor between the activity and the creatinine excretion. It is suggested that the origin of urinary angiotensin I-converting enzyme is the kidney, and that the enzyme might regulate sodium excretion in cooperation with renal kallikrein-kinin system.

Adult↗
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

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

Antihypertensive effect of the oral angiotensin I-converting enzyme inhibitor in long-term treatment of hypertensive patients.

Antihypertensive effect of an orally active angiotensin I-Converting enzyme inhibitor, SQ 14225 (Captopril) was assessed in 18 hypertensive patients, of whom 13 had essential hypertension, 2 had malignant hypertension, 2 had hypertension associated with chronic renal failure, and 1 had renovascular hypertension. Blood pressure decreased markedly not only in patients with high renin levels but also in those with low renin levels. Nevertheless, the magnitude of blood pressure reduction was correlated with the pre-treatment plasma renin activity (r =-0.64, p less than 0.01 systolic, r =- 0.60, p less than 0.05 diastolic). There was a significant correlation between the fall in mean blood pressure and the decrease in plasma aldosterone concentration 3 weeks after treatment (r = 0.64, p less than 0.05). The serum potassium elevated from 4.2 +/- 0.4 to 4.8 +/-0.9 mEq/L (p less than 0.05), and the change correlated inversely with the reduction of plasma aldosterone concentration (r = 0.71, p less than 0.02), while serum sodium slightly decreased from 140-+/- 2 to 138 +/- 3 mEq/L. There was neither finding of orthostatic hypotension nor escape from the antihypertensive effect. These results indicate that chronic inhibition of angiotensin I-converting enzyme with an orally active compound offers an effective and well-tolerated approach to treatment of hypertension.

Adult↗
PubMed1981

[Effects on the manual function of men wearing cold-protective clothing to cold stress (author's transl)].

Subjects were exposed in a climatic chamber for 60 min to air temperature at -5 degrees C, -20 degrees C and -30 degrees C wearing cold-protective clothing. The following manual functions were studied as a function of air temperature, upper limb skin temperatures, mean skin temperatures or mean body temperatures: handgrip strength, pinch strength, bolt-removing task and counting task. The decline of skin temperatures was observed during cold exposure, wearing cold-protective clothing. At 60 min of cold exposure to air temperatures at -5 degrees C, -20 degrees C and -30 degrees C, mean skin temperatures were 30.2 degrees C, 27.8 degrees C and 26.5 degrees C respectively, then II-right-finger skin temperatures were 20.7 degrees C, 13.1 degrees C and 11.8 degrees C respectively. There were reductions only on limited number of manual functions as compared with functions under normal conditions, that is, bolt-removing task and handgrip strength did not significantly change during cold exposure, whereas pinch strength and counting task decreased with lower surface temperatures and body temperatures. Body or surface cooling resulted in reductions in pinch strength by the order of 50%. The rising of the body storage index, which was calculated from the change of the mean body temperature, resulted in a linear decrease in counting task. The capacity to perform manual handling task and muscle strength appeared to vary according to the muscle used for these performance and depending on the levels of cold stress. Body cooling, combined with local upper limb cooling, produced the largest performance decrements.

Adult↗