Search PubMed⌕ Search

Biomedical subjects

M Ideishi

Publications and source records attributed to M Ideishi.

At least 55 records · Page 3Linked to original sources
PubMed1992

Influence of workload on the antihypertensive effect of exercise.

1. The relation between workload and the antihypertensive effect of exercise therapy in hypertensive patients, and the mechanism of that effect, were investigated. 2. Twenty-six patients participated in the study and were randomly assigned to 10 weeks of either low or high workload exercise. In the low workload group, 16 mild hypertensive patients were treated with bicycle ergometer exercise at approximately 50% of their maximum oxygen consumption (VO2max) for 60 min three times a week for 10 weeks. In the high workload group, 10 mild hypertensive patients exercised on the same schedule, but at approximately 75% of VO2max. 3. After 10 weeks of exercise, the low workload group had significantly lower systolic (9 mmHg), mean (6 mmHg) and diastolic (6 mmHg) blood pressures. In the high workload group, decreases in systolic (3 mmHg), mean (4 mmHg) and diastolic (5 mmHg) blood pressure were not statistically significant. 4. In the low workload group, changes in haemodynamic and humoral variables were not significant, except for a reduction in plasma norepinephrine at week 7. Cardiac index and plasma norepinephrine tended to decrease. In the high workload group, plasma norepinephrine and the renin-angiotensin system were transiently stimulated after 4 weeks of exercise. Stroke volume significantly increased (+26.4%) after 10 weeks of high workload exercise. 5. Based on these results and better patient compliance with the exercise programme in the low workload group than in the high workload group, low workload exercise therapy was recommended to mild hypertensive patients.

Adult↗
PubMed1992

Mild exercise decreases plasma endogenous digitalislike substance in hypertensive individuals.

Changes in a plasma endogenous digitalislike substance were investigated in relation to the antihypertensive mechanism of mild exercise. Fifteen women with mild essential hypertension and seven normotensive female volunteers were divided into exercised hypertensive (n = 10), nonexercised hypertensive (n = 5), and nonexercised normotensive (n = 7) groups. A 4-week general clinical observation period preceded the study period of 10 weeks. The exercised hypertensive individuals were treated with a lactate threshold exercise that corresponded to approximately 50% of the maximum oxygen consumption three times a week, whereas the nonexercised groups were observed at the outpatient clinic as control groups. In the exercised group, systolic blood pressure fell by 7 mm Hg (p = 0.05), diastolic by 6 mm Hg (p less than 0.01), and mean blood pressure by 7 mm Hg (p less than 0.01) after 10 weeks. The reduction in the plasma endogenous digitalislike substance was significant after 7 (-1.02 ng/ml, p less than 0.05) and 10 (-1.04 ng/ml, p less than 0.05) weeks in this group. It positively correlated with the reduction in diastolic (r = 0.70, p less than 0.05) or mean (r = 0.66, p less than 0.05) blood pressure and with changes in plasma norepinephrine (r = 0.76, p less than 0.05). The mean corpuscular volume of erythrocytes decreased (-1.7 fl, p less than 0.01) after 10 weeks of exercise, and the plasma volume index tended to decrease (-108 ml/m2, p = 0.28). In the control groups, significant changes in blood pressure and plasma endogenous digitalislike substance were not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1992

Cardioprotection of ACE inhibitor in ischemic heart is not dependent on the local angiotensin II formation.

Angiotensin II (AII) and bradykinin (BK) release into anterior interventricular vein (AIV) increased significantly 30 minutes after left anterior descending artery (LAD) occlusion in the absence of kidneys. Captopril enhanced BK release, but did not suppress the increase of AII release. Nafamostat suppressed both releases. Infarct size was significantly reduced by captopril but not by nafamostat. These results suggest that cardioprotective effect of captopril might be dependent on local BK accumulation, but not on suppression of local AII generation.

Angiotensin II↗
PubMed1991

Human renin activation by protease from the renin granule fraction of the dog kidney cortex.

To clarify the possible conversion of prorenin in renin granules where conversion reportedly occurred, we investigated whether the renin granule fraction of the kidney could activate prorenin to the active form. Renin granules were isolated from the dog kidney cortex by discontinuous sucrose density gradient centrifugation. Human active renin was quantified by immunoradiometric assay which could detect only the human active renin but not the inactive human renin or dog renin. Inactive renin from human amniotic fluid was incubated with the subcellular fraction of the dog kidney cortex. The renin granule fraction that showed the highest renin activity stimulated the inactive renin to become the active form. The membrane preparation obtained from the renin granule fraction by freezing and thawing the fraction in low osmolarity retained the activity of renin activation. Other subcellular fractions showed less renin activation. The optimal pH for renin activation by the membrane was pH 5.0 to 6.0. The activation depended on the time of incubation and concentration. The activation was inhibited by N-ethylmaleimide but not by EDTA or serine protease inhibitors. These results suggest that renin is processed by a membrane bound protease in renin granules.

Amniotic Fluid↗
PubMed1990

Substrate-dependent angiotensin II formation in the peripheral circulation.

An alternative angiotensin II-forming system distinct from the vascular renin-angiotensin system was demonstrated using a rat hindlimb perfusion system and synthetic substrates. This pathway was resistant to captopril and aprotinin, but was highly sensitive to chymostatin. Moreover, angiotensin II formation was substrate-dependent, i.e. angiotensin II formation from tridecapeptide human renin substrate in the presence of captopril was more than twice than that from an equimolar amount of angiotensin I. Both pathways may play a role in regulating the peripheral circulation.

Angiotensin I↗
PubMed1990

High-renin malignant hypertension secondary to an aldosterone-producing adenoma.

Malignant hypertension and high plasma renin activity was found in a 39-year-old woman with an aldosterone-producing adenoma. Only 3 similar cases have been previously reported, and all patients died before or after identification of the adenoma. The present paper documents the first reported case of a successfully managed high-renin malignant hypertension secondary to an aldosterone-producing adenoma. Regardless of its sporadic occurrence and common presence with low plasma renin activity, primary aldosteronism should be considered as a possible underlying cause of high-renin malignant hypertension.

Adenoma↗
PubMed1990

Angiotensin-converting activity of tissue kallikrein.

This study examined the ability of tissue kallikreins, purified from both rat submandibular gland (SMG) and human urine, to form angiotensin II from synthetic angiotensin I. Both kallikreins converted angiotensin I to angiotensin II at neutral pH with the following kinetic constants: SMG kallikrein, Km = 9.43 x 10(-5) mol/l, Kcat = 1.58 mumols/mg protein/min; human urinary kallikrein, Km = 1.71 x 10(-4) mol/l, Kcat = 0.06 mumol/mg protein/min. These activities were not affected by angiotensin-converting enzyme (ACE) inhibitor. These results suggest that tissue kallikrein might participate in the formation of angiotensin II during administration of an ACE inhibitor.

Angiotensin I↗
PubMed1990

Inhibitory effects of kinins on angiotensin I conversion in the local circulation.

The inhibition of angiotensin converting enzyme (ACE) by kinins was studied using bradykinin (BK), lysyl-bradykinin (Lys-BK), [Hydroxyproline3]-bradykinin ([Hyp3]-BK) and [Hydroxyproline3]-lysyl-bradykinin ([Hyp3]-Lys-BK). The latter two are novel kinins recently identified in our laboratory. All the four kinins displayed competitive inhibition on the conversion of angiotensin I to angiotensin II by purified canine lung ACE. Inhibition constants (Ki) for the four kinins were estimated from Dixon's plot as follows-BK: 0.27 microM, Lys-BK: 0.57 microM, [Hyp3]-BK: 0.34 microM, and [Hyp3]-Lys-BK: 0.27 microM. In the rat hindlimb perfusion system, the kinins were demonstrated to partially inhibit angiotensin I conversion to angiotensin II by the vascular ACE. Taken together, these results suggest that angiotensin II formation by ACE in the vascular tissue is possibly inhibited by local kinins, especially after ACE inhibitor administration. This indirect action of kinins, coupled with its direct vasodilatory action, might indicate a cooperative participation in vasodilation.

Angiotensin I↗
PubMed1989

Isolation of [hydroxyproline3]Lysyl-bradykinin formed by kallikrein from human plasma protein.

[Hydroxyproline3]Lysyl-bradykinin ([Hyp3]Lys-BK), a new kinin was isolated, besides Lysyl-bradykinin (Lys-BK), from the reaction mixture of human plasma protein Cohn's fraction IV-4 with hog pancreatic kallikrein. The liberated kinins were isolated by procedures including ethanol extraction, Sephadex G-15, CM cellulose and reverse-phase high performance liquid chromatography and quantitated by radioimmunoassay. On HPLC, two peaks of immunoreactive kinins emerged. Peak 1, an unknown kinin proceeded to peak 2 which had an identical retention time to that of Lys-BK. The amino acid sequence of the unknown peak 1 proved to be Lys-Arg-Pro-Hyp-Gly-Phe-Ser-Pro-Phe-Arg, or [Hydroxyproline3]Lys-BK, and peak 2 Lys-BK. The ratio of the amounts of two kinins thus formed were [Hyp3]Lys-BK 25 +/- 4% and Lys-BK 75 +/- 4%. The existence of [Hyp3]Lys-BK suggests a presence of a new kininogen containing [Hyp3]Lys-BK in human plasma protein.

Amino Acid Sequence↗
PubMed1988

Identification of [hydroxyproline3]-bradykinin released from human plasma and plasma protein Cohn's fraction IV-4 by trypsin.

Aside from bradykinin (BK), a novel kinin, [Hydroxyproline3]-bradykinin ( [Hyp3]-BK), was isolated from the reaction mixture of human plasma and plasma protein Cohn's fraction IV-4 with trypsin. The liberated kinins were isolated based on procedures which we previously described for the isolation of [Hyp3]-lysyl-bradykinin ( [Hyp3]-Lys-BK) formed by kallikrein. The ratio of the amounts of two kinins thus formed from human plasma protein Cohn's fraction IV-4 were [Hyp3]-BK 25 +/- 4% and BK 75 +/- 4%, similarly to that of [Hyp3]-Lys-BK and Lys-BK, formed by kallikrein, but it varied by persons. The isolation of [Hyp3]-BK and [Hyp3]-Lys-BK suggests that a novel kininogen containing hydroxyproline in the third position of the bradykinin sequence in human plasma protein, possibly undergone post-translational modifications.

Amino Acids↗
PubMed1988

Identification of [hydroxyproline3]-lysyl-bradykinin released from human plasma protein by kallikrein.

[Hydroxyproline3]-lysyl-bradykinin [( Hyp3]-Lys-BK), a new kinin was isolated, besides lysyl-bradykinin (Lys-BK), from the reaction mixture of human plasma protein Cohn's fraction IV-4 with hog pancreatic kallikrein. The liberated kinins were isolated by procedures including ethanol extraction, Sephadex G-15, CM cellulose and reverse-phase high performance liquid chromatography (HPLC) and quantitated by radioimmunoassay. On HPLC, two peaks of immunoreactive kinins emerged. Peak 1, an unknown kinin proceeded to Peak 2 which had an identical retention time to that of Lys-BK. The amino acid sequence of the unknown Peak 1 proved to be Lys-Arg-Pro-Hyp-Gly-Phe-Ser-Pro-Phe-Arg, or [Hyp3]-Lys-BK, and Peak 2 Lys-BK. The ratio of the amounts of two kinins thus formed were [Hyp3]-Lys-BK 25 +/- 4% and Lys-BK 75 +/- 4%. The existence of [Hyp3]-Lys-BK suggests a presence of a new kininogen, containing [Hyp3]-Lys-BK in human plasma protein, possibly undergone post-translational modifications.

Amino Acid Sequence↗
PubMed1987

Direct angiotensin II formation by rat submandibular gland kallikrein.

Submandibular gland kallikrein [EC 3.4.21.8] of male Sprague-Dawley rats was purified by chromatography on soybean trypsin inhibitor (SBTI)-CH-Sepharose 4B, DEAE-Sephadex A-50, aprotinin-CH-Sepharose 4B and Sephadex G-100 columns and preparative isoelectrofocusing. The molecular weight of the kallikrein was estimated to be 30,000 by Sephadex G-100 gel filtration and 29,000 by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. Isoelectric points ranged from pH 3.55 to 4.30. The kinin formed at pH 8 by this kallikrein from bovine low molecular weight (LMW) kininogen showed the same behavior as lysyl-bradykinin on HPLC in a solution of ammonium biphosphate containing acetonitrile. At physiological pH, this kallikrein also generated angiotensin II, a potent vasopressor, from human plasma protein. Rat submandibular gland kallikrein differs from tonin in the isoelectric point, the optimal pH for angiotensin II formation and the type of kinin formed. The tissue kallikrein might play a role in the regulation of local blood flow in view of its ability to form both vasoconstrictive and vasodilatory peptides.

Angiotensin II↗
PubMed1985

A case of hyperreninemic hypertension with unilateral hydronephrosis.

A patient with unilateral ureteral obstruction by urolithiasis at the ureteropelvic junction was accompanied by hypertension. Plasma renin activity (PRA) was high in peripheral veins and was significantly higher in the renal vein drained from the affected kidney than the contralateral. Infusion of angiotensin II antagonist or an oral administration of captopril, an angiotensin converting enzyme (ACE) inhibitor, resulted in a prompt drop of blood pressure. After pyelolithotomy was successfully performed, both the blood pressure and peripheral PRA completely normalized. It is suggested that the renin-angiotensin system might have played a major role in the mechanism of the accompanied hypertension. Hyperreninemia could have been caused by both renal ischemic vasoconstriction, which might be due to uretero-renal reflex, and increased synthesis of prostaglandins resulting from ureteropelvic obstruction.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1978

An accelerated hypertension with neither malignant nephrosclerosis nor elevation of plasma renin activity.

A case of accelerated hypertension, which was unique in a resistance to an angiotensin antagonist, and a lack of the elevation of plasma renin activity (PRA) is reported. Non-elevated PRA was coincided with non-malignant nephrosclerosis in renal histology. The acceleration was attributed to the neurological cause i.e., cerebral hemorrhage in the right hypothalamus which extended to the ventricle and subarachnoid space. The case therefore clinically seemed malignant-like, but it was not malignant hypertension in the sense of Volhard's classical definition. This does not conflict with the usefulness of the determination of PRA in the diagnosis of malignant hypertension with nephrosclerosis.

Aged↗
PubMedDate not supplied

A case of a clinically "silent" pheochromocytoma.

A case of a clinically "silent" pheochromocytoma is presented. The adrenal mass was incidentally discovered by abdominal ultrasonography and computed tomography. In the course of hospitalization, the patient was normotensive and asymptomatic. Plasma catecholamine levels were nearly normal, whereas urinary levels of catecholamine metabolites were slightly elevated. A glucagon provocative test and 131I-metaiodobenzylguanidine scintigram were useful for diagnosing such an atypical pheochromocytoma. A discussion of clinically-unsuspected pheochromocytoma is also presented.

3-Iodobenzylguanidine↗
PubMedDate not supplied

Effects of a new calcium channel blocker, TA 3090, on serum lipoprotein levels in mild to moderate essential hypertension.

The 25 hypertensive patients received 20 to 40 mg of TA 3090 daily for 12 weeks. Blood pressures declined significantly during treatment, from a mean of 162/98 to 145/88 mmHg. There were no significant changes in levels of total or very low-density lipoprotein cholesterol or triglyceride, in levels of low-density lipoprotein cholesterol, high-density lipoprotein (HDL) cholesterol, HDL2 cholesterol, HDL3 cholesterol, or in levels of apolipoprotein (apo) B, C-II, C-III, or E. Apo A-I and A-II levels increased significantly from 130 and 29.2 mg/dl before treatment to 152 and 31.4 mg/dl at 12 weeks. Mean serum creatinine levels decreased significantly from 0.92 to 0.80 mg/dl. No other drug-related changes in laboratory test results or side effects were noted. It is concluded that TA 3090 is a safe and effective treatment for mild to moderate hypertension.

Adult↗