Biomedical subjects

S Matsuki

Publications and source records attributed to S Matsuki.

At least 91 records · Page 5Linked to original sources

PubMed1976

Benign desoxycorticosterone-producing adrenal tumor.

A woman with a benign tumor of the left adrenal cortex had a six-year history of hypertension. Serum potassium level and plasma renin activity were low. Plasma aldosterone and cortisol levels were low normal, and plasma desoxycorticosterone (DOC) level was extremely high. Iodine 131-labeled cholesterol accumulated in the tumor in the left upper quadrant of the abdomen. At laparotomy, a benign adrenal tumor was excised; thereafter, the blood pressure and plasma DOC levels returned to normal. We believe that this is the first case of a benign DOC-producing adrenal tumor.

Adrenal Gland Neoplasms↗

PubMed1976

Effects of furosemide and chlorothiazide on blood pressure and plasma renin activity.

Short (2 weeks) and long (12 weeks) term effects of furosemide and chlorothiazide on blood pressure, plasma renin activity, and uric acid concentration were studied in 69 hypertensive patients. Both treatments caused significant reductions in blood pressure and increases in plasma renin activity and uric acid at 2 and 12 weeks in 6) normal renin patients; there was no difference between the effects of furosemide and that of chlorothiazide. Reduction in blood pressure in eight low renin patients who showed smaller changes in plasma renin activity and uric acid was not significant at 2 weeks but significant after 12 weeks of treatment.

Adult↗

PubMed1976

The mechanism of low-renin hypertension: aldosterone response to sodium restriction and upright posture, angiotensin II, ACTH and potassium in patients with hypertension.

Plasma renin activity and aldosterone were measured simultaneously in 67 out-patients with essential hypertension. High aldosterone was more often in patients with high renin, and low levels of aldosterone were usual in those with low and normal renin. In order to study the mechanism by which aldosterone and renin acitvity are suppressed in low-renin hypertension, 25 patients (13 normal-renin hypertensives, 10 low-renin patients including 4 non-responders and two DOC excess hypertensives) were investigated as inpatients. Plasma renin activity, aldosterone and cortisol were determined by the following stimualtions with 3 days of sodium restriction and 2 hours of upright posture, angiotensin II infusion (at a dose which increased 20mmHg of diastolic blood pressure), ACTH administration (rapid i.m. injection of 0.25 mg of alpha 1-24 preparation) and potassium infusion (30 meq of potassium i.v.). Responses of aldosterone in normal-renin hypertensives to all stimulations were 3-5 fold increases from bases line values. Low-renin hypertensives except two of four non-responders showed the responses similar to those in normal-renin patients. The responses of two of the non-responders were similar to those in DOC excess hypertensives who showed reduced responses of aldosterone to some of these stimulations. Thus, it seems that low-renin hypertension is a clinical entity caused by a variety of mechanisms, and the mechanism by which low-renin hypertension is induced is not explained by one factor such as an unknown mineralocorticoid.

Adrenocorticotropic Hormone↗

PubMed1975

[Effects of low salt plus upright posture, angiotensin II, ACTH, and potassium upon plasma renin activity, aldosterone, and cortisol (author's transl)].

In order to study the control system of plasma aldosterone in human, we examined the effects of low salt plus upright posture, angiotensin II, ACTH and potassium upon plasma renin activity, aldosterone and cortisol in five subjects who were supposed to be normal. All of the procedures, low salt diet with below 3 g of salt and 2 hr-upright posture, 0.25 mg of Cortrosyn, angiotensin infusion to increase 20mmHG of diastolic pressure for an hour, and 30 mEq of potassium infusion stimulated plasma aldosterone significantly. Furthermore, in each subject the degrees of response to each of these stimulations were almost same. In an old woman aged 68, responses to all of stimulations were significantly lower than those in other subjects. Plasma cortisol was significantly stimulated by ACTH, but slightly reduced by potassium infusion. From these results, it is certain that plasma aldosteron levels are easily affected by a small amount of changes in angiotensin, ACTH, potassium and sodium. However, responses of aldosterone to these changes seem to be decreased in old subjects.

Adrenocorticotropic Hormone↗

PubMed1975

The effects of cyclic AMP, theophylline, angiotensin II and electrolytes upon renin release from rat kidney slices.

The effects of cyclic AMP, theophylline, angiotensin II and electrolytes upon renin release were examined by incubation of rat kidney slices. Angiotensin inhibited renin release with increasing concentrations. On the other hand, cyclic AMP and theophylline stimulated it. Calcium also seemed to play an important role in the control of renin release from kidney slices. However, the direct effects of sodium and potassium upon renin release were not conspicuous.

Angiotensin II↗

PubMed1974