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Biomedical subjects

T Saruta

Publications and source records attributed to T Saruta.

At least 487 records · Page 27Linked to original sources
PubMed1986

Central and peripheral contributions of the renin-angiotensin system in two models of experimental hypertension in rats.

To examine the relationships between the central and peripheral renin angiotensin system in normotensive Wistar Kyoto (WKY) rats, two-kidney, one-clip Goldblatt renovascular hypertension (RVH), spontaneously hypertensive rats (SHR), SQ 14225 (captopril) was administered intraventricularly (IVT) and intravenously (IV) in the alternative manner and their combination. Also, the effects of IVT captopril on the peripheral sympathetic nervous system were evaluated using an intravenous injection of prazosin. IVT captopril induced a significant reduction of blood pressure in both types hypertensive rats but not in normotensive rats. Greater depressor effects of IV captopril not IV prazosin following IVT captopril were observed in RVH compared to those in SHR. These results indicate that the pressor action of the brain renin angiotensin system is closely related with the sympathetic nervous system in hypertensive conditions and that these functions are independent from the peripheral renin angiotensin system. Furthermore, their roles were different in different types of experimental hypertension in rats.

Animals↗
PubMed1986

Serum creatine kinase release and alpha- and beta-adrenergic receptors.

Changes in the serum creatine kinase (CK) activity and the mechanism of its release after administration of two kinds of beta-blockers to rats were studied in order to determine the mechanism of the increase in serum CK accompanying administration of beta-blockers. When pindolol or propranolol was administered at a dose of more than 10 mg/kg of body weight, the serum CK activity was increased in proportion to the dose. Also when an alpha-stimulator or an alpha, beta-stimulator such as noradrenaline and adrenaline was administered, the serum CK activity was increased. When the beta-stimulator isoproterenol or the alpha 1-blocker prazosin was administered, there was no increase in the serum CK activity. In terms of consecutive administration of a combination of beta-blockers and adrenaline, the serum CK activity was not increased by the second and succeeding administrations. As for the use of adrenaline alone, on the other hand, the serum CK activity after the second administration was equal to that after the first administration. The increase in CK activity after administration of adrenaline as the second treatment following administration of a beta-blocker as the first treatment was approximately the same as that after single administration of adrenaline. From the fact that the serum CK activity in rats was increased by administration of an alpha-stimulator and of a beta-blocker, it is possible that CK release in the blood is due to the action of alpha-receptors rather than beta-receptors. In the case of consecutive administration of a beta-blocker, the serum CK activity was not increased after the second administration. However, the serum CK activity was increased by the administration of an alpha-stimulator. This finding suggests the possibility that CK release is due to the disturbance of the balance between alpha-receptor and beta-receptor. Most of the CK isoenzymes released in the blood after administration of a beta-blocker were of the MM type.

Animals↗
PubMed1986

Unusual apparent hyperchloremia induced by long-term abuse of bromide-containing drugs.

Recently, we have observed 8 cases showing unusually high serum chloride (Cl-) levels of 282, 279, 257, 251, 213, 169, 123 and 120 mEq/l respectively, as measured by the ion selective electrical method (ISE). All of these cases showed almost normal Cl- levels by the coulometric method. Five of the patients had been taking Bromide (Br-)-containing drugs for a long period, and were found to have high serum levels of Br- ranging from 0.6 to 11.0 mEq/l (normal level: 0.1 mEq/l greater than). The cause of this abnormal elevation in serum Cl- as measured by ISE was investigated as follows. First, normal human pooled serum was mixed with NaBr solution to give increasing concentrations of Br- ions, which was then analyzed using the ISE method. Results showed that the selective response ratio of Br- against Cl- had values as high as 15.03 with ISE in contrast to values of 1.0 obtained by coulometry. Secondly, 7 healthy volunteers were given 4 commercially obtained Br(-)-containing tablets (Sedes A; Shionogi & Co., Ltd.) every day for 8 days. Their mean serum Cl- values measured by ISE gradually increased from 108 to 112 mEq/l, paralleling increments of mean Br- value from 0.1 to 0.6 mEq/l over 9 days. From these observations, it is concluded that serum chloride values obtained by ISE are easily interfered with by Br-. Paradoxically, however, this fact is often a good indicator of Br- intoxication. The authors therefore recommend clinicians to pay more attention to the Br- intoxication that often occurs from overdosage of Br(-)-containing drugs, some of which are commercially available without prescription.

Adult↗
PubMed1985

Depressor effects of captopril in DOCA-salt hypertensive rats: role of vasopressin.

Oral administration of the angiotensin I-converting enzyme inhibitor captopril produced a substantial reduction of blood pressure in DOCA-salt hypertensive rats. After oral administration of captopril (30 mg/kg), mean blood pressure decreased from 172 +/- 11 to 148 +/- 9 mmHg (P less than 0.01) in one hour and its antihypertensive effects lasted for the next seven hours. Plasma vasopressin levels showed a marked elevation in DOCA-salt hypertensive rats compared with control values (22 +/- 5 versus 5 +/- 3 pg/ml). This increase in vasopressin was significantly reduced by captopril from 25 +/- 5 to 8 +/- 6 pg/ml. In addition, whole body vascular reactivity to norepinephrine was examined. Responsiveness was at first attenuated but returned to control value in spite of reduction of both plasma vasopressin and blood pressure. Thus, captopril reduces blood pressure in DOCA-salt hypertensive rats and the fall in blood pressure is accompanied by reduction of plasma vasopressin and attenuation of vascular reactivity.

Animals↗
PubMed1985

The effect of age on blood pressure in hyperthyroidism.

To better define the effect of age on blood pressure in patients with hyperthyroidism, the blood pressures of 321 patients with hyperthyroidism were compared with those of 324 euthyroid controls. Subjects were divided into four age groups by decade from 20 to 59 years. The systolic, but not diastolic, blood pressure in the patients with hyperthyroidism was significantly higher in all age groups. Among the euthyroid controls, the systolic blood pressure increased with age. However, no age-related increase was apparent among the hyperthyroid patients because of the relatively high systolic blood pressure in young patients. Effective antithyroid treatment reduced the systolic blood pressure significantly in hyperthyroid patients. The reduction of systolic blood pressure was greater in the younger hyperthyroid patients than that in the older ones, so that an age-related increase in systolic blood pressure was present after a euthyroid state had been achieved. These results provide evidence against the report that in hyperthyroidism, hypertension tends to occur in older patients, and suggest that the effect of excessive thyroid hormone on the systolic blood pressure may differ according to age.

Adult↗
PubMed1985

Effect of the angiotensin converting enzyme inhibitor, captopril (SQ14,225), on orthostatic sodium and water retention in patients with idiopathic edema.

Captopril (SQ14,225), an orally administered angiotensin converting enzyme inhibitor, was given to 8 patients with idiopathic edema, in order to study the role of the renin-angiotensin-aldosterone system in orthostatic sodium and water retention. Compared to 5 normal subjects, patients with idiopathic edema showed significantly greater reduction in water and sodium excretion, and greater increment in plasma aldosterone and plasma renin activity, in the upright posture. Captopril significantly restored water and sodium excretion, attenuated the increment in plasma aldosterone, and enhanced the rise in plasma renin activity in patients with idiopathic edema. The effects of captopril on these variables were not remarkable in normal subjects. These results suggest that an enhanced response of the renin-angiotensin-aldosterone system to standing plays an important role in the pathophysiology of idiopathic edema.

Adult↗
PubMed1985

Metoclopramide in the diagnosis of pheochromocytoma.

Cardiovascular and plasma catecholamine responses to metoclopramide (MCP), a dopamine antagonist, were examined in 5 patients with pheochromocytoma, 12 patients with essential hypertension (EHT) and 9 normotensive (NT) subjects who displayed symptoms suggestive of pheochromocytoma on a constant daily intake of 100 mEq sodium and 80 mEq potassium. Significant pressor responses to intravenous doses of 5 mg of MCP, which produced no serious pressor episodes and no other undesirable side effects, were found only in the patients with pheochromocytoma, in contrast to the subjects with EHT and NT who tended to display slight depressor responses. After curative surgery for pheochromocytoma, the MCP-induced pressor effects returned to normal. Furthermore, the enhanced pressor effects of MCP in the patients with pheochromocytoma were associated with increased plasma norepinephrine (NE) concentrations. However, the plasma epinephrine (E) concentrations remained unchanged after the MCP injection. Thus, this dose of MCP appears to be a more suitable vasopressor provocative agent in the pharmacological diagnosis of pheochromocytoma compared to currently used agents.

Adolescent↗
PubMed1985

Numerous mast cells in an 11-deoxycorticosterone-producing adrenocortical tumor. Histologic evaluation of benignancy and comparison with mast cell distribution in adrenal glands and neoplastic counterparts of 67 surgical specimens.

Pathologic study of a rare 11-deoxycorticosterone-producing adrenocortical tumor causing primary aldosteronismlike signs and symptoms, revealed several characteristic features as follows: (1) fairly large size with histologic features corresponding to those of benign zone glomerulosa-type aldosteronoma, (2) lack of spironolactone (S) bodies despite S administration, and (3) heavy mast cell infiltration. In order to explain this rare histology, the localization of mast cells in the adrenal glands and functioning adrenocortical tumors of 67 surgical specimens were investigated. The results of the study supported the view that detection of mast cells helps in the differentiation of mineralocorticoid-producing tumors from cortisol-producing ones, and that the observed mast cell infiltration was due, in part, to its production of 11-deoxycorticosterone.

Adrenal Cortex Neoplasms↗
PubMed1984

Studies on the effect of prazosin on blood pressure and serum lipids in Japanese hypertensive patients.

The introduction of the western diet and lifestyle to Japan has been associated with changes in body build, lipid levels, and disease pattern. An increased incidence of coronary heart disease parallels increased fat intake. Thiazide diuretics and beta blockers may have adverse effects on blood lipids in man leading to an increase in the risk of coronary heart disease; therefore, for many patients these drugs may not offer the optimum treatment strategy. Hence, prazosin, a drug that effectively lowers blood pressure without adversely affecting lipid metabolism, has been evaluated in nine studies within Japan. Prazosin showed adequate antihypertensive effects even at doses as low as 1 to 3 mg per day. Sustained constant blood pressure reductions were achieved with maintenance doses of 3 to 6 mg per day without significant side effects. Even when given in low doses, prazosin increased high-density lipoprotein cholesterol while inhibiting elevations of total cholesterol and decreasing triglycerides. In view of these findings, prazosin as a single agent can be considered for monotherapy of hypertension.

Blood Pressure↗
PubMed1984

Plasma prolactin, renin and catecholamines in young normotensive and borderline hypertensive subjects.

It has been reported that patients with essential hypertension have high plasma prolactin levels and suggested that reduced central dopaminergic activity may be a factor in the pathogenesis of essential hypertension. This study examines the influence of posture on plasma prolactin, plasma catecholamines, plasma renin activity, blood pressure and heart rate in 24 patients with borderline hypertension (age 19 +/- 1 years) and 20 normotensive subjects matched for age and body mass index. Supine plasma prolactin levels were similar in both groups [borderline hypertension, 11.3 +/- 0.7 ng/ml; normotensive, 10.7 +/- 0.8 ng/ml (mean +/- s.e.m.)] and no increase in plasma prolactin was observed after 10 min standing in both groups. Normotensive and borderline hypertensive subjects had similar values for supine and upright plasma renin activity and plasma norepinephrine. There were no significant correlations between supine plasma prolactin and supine blood pressure, supine plasma renin activity or plasma norepinephrine when data from both normotensive and borderline hypertensive subjects were combined. These results may provide indirect evidence against the occurrence of reduced central dopaminergic activity in borderline hypertension.

Adult↗
PubMed1984

Excretion and metabolism of dopa and dopamine by isolated perfused rat kidney.

The renal metabolism and handling of dopa and dopamine were studied with the use of the isolated perfused rat kidney to elucidate the source of urinary dopamine. Dopa added to the perfusate was rapidly metabolized, and a significant amount of urinary dopamine excretion was observed, whereas dopa was not detected in the urine. When the perfusate dopa concentration was near the plasma dopa concentration in normal rats, urinary dopamine excretion was comparable with physiological values. Carbidopa, a dopa decarboxylase blocker, added to the perfusate markedly reduced the urinary excretion of dopamine. When the physiological concentration of dopamine was added to the medium, the perfusate dopamine rapidly decreased and urinary dopamine excretion was much less than that seen in normal rats. In studies with nonfiltering kidneys, a marked decrease of dopa and slight increase of dopamine in the perfusate were observed. It is suggested that the process of glomerular filtration and tubular reuptake of dopa is not essential for renal dopamine formation. These data indicate that urinary free dopamine is mainly derived from plasma dopa, which is converted by dopa decarboxylase in the kidney.

Animals↗
PubMed1984

Hypokalemia and prostaglandin overproduction in Bartter's syndrome.

In 2 adult patients with Bartter's syndrome, in whom chloride reabsorption at the diluting segment of the nephron was markedly reduced, serum potassium concentration could be improved with oral administration of a large amount of potassium chloride. In both cases, improvement of serum potassium levels with oral potassium load resulted in an increase in plasma renin activity (PRA) and plasma aldosterone concentration (PAC), a decrease in urinary excretion of prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha), and an improvement of pressor responsiveness to angiotensin II and norepinephrine. Treatment with indomethacin also improved the pressor responsiveness to angiotensin II and norepinephrine, but this occurred in association with a decrease in PRA, PAC and urinary excretion of PGE2 and PGF2 alpha. These results indicated that an event at the renal tubular level leading to potassium depletion is the most proximal pathogenetic defect in Bartter's syndrome, and that this in turn contributes to excessive prostaglandin production leading further to the decreased pressor responsiveness to vasoactive substances.

Aldosterone↗
PubMed1984

Aldosterone responses to angiotensin II, adrenocorticotropin, and potassium in chronic experimental diabetes mellitus in rats.

To investigate alterations in aldosterone secretion in diabetes mellitus, the effects of angiotensin II, ACTH, and potassium on aldosterone secretion were examined in conscious unrestrained streptozotocin-induced diabetic rats (60 mg/kg, 12 weeks before study). In chronic experimental diabetic rats where PRA, plasma aldosterone concentration, and urinary excretion of prostaglandin E2 were significantly decreased, a significant attenuated response of aldosterone secretion was demonstrated after infusion of angiotensin II, ACTH, or potassium. Yet the plasma fluorogenic corticosteroids response to ACTH in diabetic rats was not significantly different from that in control rats. After acute potassium infusion (0.30 meq/kg X min), plasma potassium levels in diabetic rats were significantly higher than in control rats, although immunoreactive insulin levels remained unchanged compared to the significant elevation in control rats. These results suggest that defects in aldosterone synthesis exist in chronic experimental diabetic rats and that potassium homeostasis is impaired during acute potassium loading. This change in potassium homeostasis may be related to both insulin and aldosterone deficiencies.

Adrenal Cortex Hormones↗
PubMed1984

Potassium homeostasis in chronic experimental diabetes mellitus in rats.

To examine potassium homeostasis in diabetes mellitus, we observed the effect of dietary potassium loading on the renin-angiotensin-aldosterone system and potassium balance in streptozotocin-induced diabetic rats. In diabetic rats with 26.51 +/- 1.89 mmol/l of serum glucose, the plasma renin activity (PRA), plasma aldosterone (PA), immunoreactive insulin (IRI) and urinary excretion of prostaglandin E2 (PGE2) were all significantly lower than in control rats, but the plasma potassium and renal function were not significantly different. With potassium loading, both control and diabetic rats showed a similar increase in plasma potassium and urinary potassium excretion and a decrease in PRA, but the IRI, plasma corticosterone and urinary excretion of PGE2 exhibited no significant change. On the other hand, the PA was significantly increased only in the control rats, and not in the diabetic rats on potassium loading. Based up on these results, it is suggested that potassium homeostasis is well maintained in diabetic rats with normal renal function in spite of an attenuated response of aldosterone secretion to dietary potassium loading and insulin deficiency.

Aldosterone↗
PubMed1984

Modulation of aldosterone secretion in frusemide-induced hypokalaemia.

To study the effect of hypokalaemia in the regulation of aldosterone secretion, repeated injections of frusemide (3 mg/kg) plus saline with or without simultaneous infusion of potassium chloride (1 mEq/kg/h) were performed in 24 conscious female rabbits for 7 h. Without potassium supplementation, the plasma renin activity (PRA) remained elevated throughout the study, while an initial increase (1 h to 3 h) in plasma aldosterone (PA) gradually returned to normal with reduction of the serum potassium. In rabbits on potassium supplements to prevent the development of hypokalaemia, both PRA and PA remained elevated. The incremental aldosterone response to administration of potassium chloride, angiotensin II or ACTH, was considerably smaller in potassium-depleted rabbits than in potassium-repleted rabbits. These results suggest that serum potassium modulates the effects of angiotensin II or ACTH on aldosterone secretion, and that a certain level of potassium is necessary to maintain the aldosterone secretory capacity of the adrenal gland.

Adrenocorticotropic Hormone↗