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Biomedical subjects

R Takeda

Publications and source records attributed to R Takeda.

At least 487 records · Page 27Linked to original sources
PubMed1979

Reduced response of plasma aldosterone to acute ACTH stimulation during long-term treatment with spironolactone in essential hypertension.

The response of plasma aldosterone (PA) to ACTH administration (250 micrograms alpha 1-24 ACTH i.m.) before and during treatment with spironolactone (Sp, 75--100 mg/day) for at least 8 months was studied in 11 patients with essential hypertension. These responses were compared with those before and during prolonged treatment with hydrochlorothiazide (Th, 50--75 mg/day), with or without potassium supplement, in 14 hypertensives. PA and plasma cortisol (PC) were determined by radioimmunoassay in which Sp showed minimal cross-reactivity. Both Sp and Th treatments caused similar increases in plasma renin activity accompanied by nearly identical decreases in blood pressure and body weight. PA was also increased by both treatments, but to a significantly greater extent in the Sp-treated group. Serum potassium concentration was increased only by Sp treatment. The response of PA, but not of PC, to acute ACTH stimulation was blunted in the Sp-treated group. That is, the maximal increment of PA above the baseline level was significantly lower during Sp treatment than either before Sp treatment of during Th treatment. These results demonstrate that long-term treatment with Sp can inhibit aldosterone production by acute ACTH stimulation in patients with essential hypertension.

Adrenocorticotropic Hormone↗
PubMed1979

Selective hypoaldosteronism with hyperreninemia in a diabetic patient.

A 62-yr-old diabetic woman exhibited low plasma and urinary aldosterone levels in the face of markedly elevated PRA during the course of nonketoacidotic hyperglycemic precoma with dehydration, hyponatremia, and hyperkalemia, for which she was hospitalized. Studies performed after her recovery from precoma revealed hyperreninemic hypoaldosteronism with normal adrenoglucocorticoid function. While the patient was supine, PRA on a 256-meq sodium intake was at or above the upper limit of the normal range for a 200-meq sodium intake; furthermore, after sodium depletion with furosemide and 4 h of ambulation, PRA markedly increased. No increases in plasma inactive renin were found. Plasma renin substrate concentration was normal. Plasma levels and urinary excretion of aldosterone were low and increased slightly during sodium restriction with insulin treatment, accompanied by hyperkalemia and sodium loss, despite markedly elevated PRA. Repository ACTH administration induced sodium retention and potassium loss with a normal increase in urinary 17-hydroxycorticosteroids. Plasma levels of deoxycorticosterone, corticosterone, and 18-hydroxycorticosterone were normal, while plasma aldosterone was low. Levels of these mineralocorticoids remained unchanged during angiotensin II infusion on both 256-meq and 100-meq sodium intakes. Rapid ACTH administration produced normal increases in plasma deoxycorticosterone and corticosterone but caused a subnormal increase in plasma aldosterone. These results suggest adrenal insensitivity to angiotensin II, possibly a defect in adrenal angiotensin II receptors, as the cause of hypoldosteronism with hyperreninemia in this patient.

Aldosterone↗
PubMed1979

Prolonged pseudoaldosteronism induced by glycyrrhizin.

We describe the natural recovery from the aggravated hypertension, hypokalemia and suppression of the renin-aldosterone axis after the glycyrrhizin discontinuation in two mild hypertensive women aged 71 and 68 years, who had been administered 273 to 546 mg glycyrrhizin daily for 1.5 and 6 months, respectively, for the treatment of liver disease. About one month after the glycyrrhizin discontinuation, acceleration of hypertension, hypokalemia and suppression of the renin-aldosterone system still continued in both patients. At this stage, sodium restriction resulted in the normalization of blood pressure with weight loss and the subsequent sodium repletion produced a rapid increase in blood pressure to hypertensive levels observed before sodium restriction, with weight gain. Plasma renin activity and plasma aldosterone were low and did not respond to sodium restriction. Inappropriately excessive amounts of potassium were also excreted in the presence of hypokalemia. About one and a half months later, the improvements of aggravated hypertension, hypokalemia and suppressed renin-aldosterone system gradually occurred in both patients. Sodium restriction performed about three months later in case 2 no longer produced the changes in blood pressure and body weight. Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. These results demonstrate that both patients had a prolongation of the syndrome resembling primary aldosteronism except the low plasma aldosterone level about one month after the glycyrrhizin discontinuation. The possible mechanisms by which this prolongation was caused are discussed.

Aged↗
PubMed1979

Effects of oxandrolone on plasma lipoproteins in patients with type IIa, IIb and IV hyperlipoproteinemia: occurrence of hypo-high density lipoproteinemia.

The effects of oxandrolone on plasma lipids and lipoprotein composition in patients with type IIa, IIb and IV hyperlipoproteinemia were investigated. Oxandrolone (4 mg/day, for 28 days) induced a significant reduction in plasma and VLDL triglyceride. Reciprocal elevation of LDL cholesterol was observed in 8 of 10 type IV patients and in 2 of 5 type IIb patients. In patients with type IV hyperlipoproteinemia, significant reduction of plasma apolipoproteinB and VLDL apolipoprotein B and inverse LDL apolipoprotein B increment was observed after treatment with oxandrolone. HDL cholesterol was decreased. Hypo-high density lipoproteinemia defined as HDL cholesterol concentration below 40 mg/100 ml occurred in 7 of 10 type IV, 3 of 6 type IIb and 1 of 4 type IIa patients.

Adult↗
PubMed1979

The action of acetaldehyde on the intracellular electrical activities of the guinea-pig taenia coli.

The effect of acetaldehyde on the membrane potential and the membrane resistance of the guinea-pig taenia coli has been studied with an intracellular recording technique. Application of acetaldehyde in the concentration of between 5 and 20 mM produces reduction or elimination of the spontaneous spike activity and hyperpolarization of the membrane. The amplitude and the rates of rise and fall of the action potential are reduced by the drug. The duration of the spike is slightly prolonged. Acetaldehyde also reduces the amplitude of the evoked action potential produced by externally applied cathodal stimulation in twice hypertonic solution. Electronic potentials induced by anodal current are reduced both in size and time course by acetaldehyde during the stage of hyperpolarization.

Acetaldehyde↗
PubMed1978

[Plasma renin activity response to isometric handgrip exercise in normotensive and hypertensive patients (author's transl)].

1) Plasma renin activity (PRA) response to isometric exercise was studied before and after the intravenous administration of 0.2 mg/kg of propranolol in 8 normotensive and 10 normal renin hypertensive patients. 2) Handgrip exercise at the 30% level of maximal voluntary contraction (MVC) for four minutes induced a significant increase in PRA in either normotensive or normal renin hypertensive patients, while the increase in PRA in normal renin hypertensive patients was significantly higher than that in normotensive patients. 3) Pretreatment with the administration of propranolol inhibited an increase in PRA after handgrip exercise in either normotensive or normal renin hypertensive patients. 4) The results suggest that isometric handgrip exercise can induce an augmentation in renin release mainly by stimulation of the sympathetic nervous system in either normotensive or normal renin hypertensive patients. The possible mechanism of the exaggerated response in PRA to handgrip exercise in normal renin hypertensive patients has been discussed.

Adolescent↗