Biomedical subjects
Publications and source records attributed to T Saruta.
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The effects of four different diuretics, hydroflumethiazide, furosemide, piretanide and potassium canrenoate on the vascular responses to norepinephrine and potassium chloride in the perfused rat mesenteric vascular bed have been studied. Furosemide or piretanide in the perfusate inhibited the vascular response to norepinephrine in a dose-related manner, while the vascular contraction induced by potassium chloride was not affected by these substances. In contrast to furosemide and piretanide, potassium canrenoate inhibited vascular responses to both norepinephrine and potassium ions. Hydroflumethiazide did not induce any change in the vascular response to norepinephrine or to potassium chloride. From these results, it is suggested that furosemide, piretanide and potassium canrenoate, but not hydroflumethiazide have direct vascular actions independent from their renal actions which may contribute to their antihypertensive effects.
The effects of three types of angiotensin-converting enzyme inhibitor, SQ 14225 (captopril), SQ 20881 (teprotide) and SA 446 (Santen, Osaka, Japan), on the vascular contraction induced by norepinephrine were studied in the perfused rat mesenteric vascular bed. (1) SQ 14225 attenuated in the vascular contraction induced by norepinephrine, but SQ 20881 and SA 446 revealed no effect on vascular reactivity. (2) The effect of SQ 14225 was not altered in the presence of bradykinin or angiotensin II in the perfusate. On the basis of these results it is suggested that the attenuating effect on the vascular response to norepinephrine may be limited to SQ 14225 and that its effect is not mediated through the renin-angiotensin or kallikrein-kinin system.
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1. The role of the kidney and vasopressin in the increase of blood pressure obtained when angiotensin II is injected intraventricularly into rats has been investigated. 2. Intraventricular injection of angiotensin II led to a significant increase in blood pressure in the control and all sham-operated rats compared with that in unilaterally nephrectomized, one-kidney denervated rats and bilaterally nephrectomized rats. The degree of increase in blood pressure in unilaterally nephrectomized, one-kidney denervated rats was equal to that in bilaterally nephrectomized rats. 3. The increase in blood pressure in the bilaterally nephrectomized rats lasted significantly longer than that in the control and unilaterally nephrectomized, one-kidney denervated rats. 4. In the bilaterally nephrectomized rats plasma vasopressin was still higher 30 min after the intraventricular injection of angiotensin II than that of the control and unilaterally nephrectomized, one-kidney denervated rats. 5. These results suggest that the rise in blood pressure observed after intraventricular injection of angiotensin II is due partly to stimulation of the renal sympathetic nervous system and partly to increase in plasma vasopressin concentration.
A 38-year-old woman had polyarthralgia, proteinuria, and intractable diarrhea. Biopsy of the synovium, and intractable diarrhea. Biopsy of the synovium, rectal mucosa, and kidney revealed abundant deposition of amyloid, and the diagnosis of primary amyloidosis was made. The joint symptoms and diarrhea subsequently subsided, but her renal function progressively deteriorated. Maintenance hemodialysis was started 3 1/2 years later and was successfully continued for five years without major complications except for osteonecrosis of the femoral heads. Her Brescia shunt, however, failed frequently until a polytetraflouroethylene shunt was installed. Although the prognosis of primary amyloidosis and renal failure is poor, our case illustrates that persistent remission of the extrarenal symptoms can take place and that these patients can be successfully maintained by hemodialysis.
The role of the renin-angiotensin system in the regulation of the blood pressure of dexamethasone-treated rats (Dex) was evaluated using saralasin, an angiotensin II antagonist, and SQ 14225 (SQ) (d-3-mercapto-2-methylpropranoyl-1-proline), an angiotensin-converting enzyme inhibitor. During a 7-day period blood pressure rose 65 +/- 10 mmHg (P less than 0.001) in Dex with no significant changes in plasma renin activity. Concurrent administration of dexamethasone and SQ attenuated the elevation of blood pressure (P less than 0.05). In the conscious, freely moving state, intravenous injection of SQ (10, 30, 100 micrograms/kg) reduced blood pressure of DEX in a dose-dependent manner (P less than 0.05). Also, intravenous injection of saralasin (10 micrograms.kg-1 . min-1) reduced blood pressure significantly (P less than 0.01). Bilateral nephrectomy abolished the effects of saralasin and SQ on blood pressure in Dex. These results indicate that the elevation of blood pressure in DEX depends partially on the renin-angiotensin system.
The role of the renin-angiotensin system in polyuric patients was studied in 5 patients with pituitary diabetes insipidus, 1 patient with nephrogenic diabetes insipidus and 3 patients with psychogenic polydipsia by determining the plasma renin activity and infusing an angiotensin II analog, 1-Sar, 8-Ile angiotensin II. In all patients with diabetes insipidus, plasma renin activity was markedly increased and the blood pressure was reduced in 5 of 6 patients by the administration of the angiotensin II analog. In the other patient, the blood pressure remained unchanged. The plasma renin activity and response of blood pressure to the angiotensin II analog in a patient with nephrogenic diabetes insipidus were not significantly different from there of patients with pituitary diabetes insipidus. On the other hand, in all patients with psychogenic polydipsia, plasma renin activity was normal or low, and the blood pressure increased with the administration of the angiotensin II analog. These results suggest that evaluation of the renin-angiotensin system by determining plasma renin activity and infusing an angiotensin II analog is useful in differentiating between diabetes insipidus and psychogenic polydipsia.
The site of action in the steroidogenic pathway of aldosterone stimulating factor (ASF), isolated from human urine, was studied in collagenase-dispersed rabbit adrenal capsular cells and compared with those of beta-lipotropin (beta-LPH), angiotensin II (A II) and adrenocorticotropic hormone (ACTH). When incubated with adrenal cell suspension at 37 degrees C for 2 hours, ASF, beta-LPH and ACTH induced dose-related increases in aldosterone production. ASF was less potent (ED50 = 10(-9) M) than ACTH but was more potent than beta-LPH. When ASF was added to the incubation with low dose of A II or ACTH, its effect on aldosterone production was additive, while no additional effect of ASF on aldosterone production was obtained in the presence of high dose of A II or ACTH. ASF increased the conversion of corticosterone to aldosterone like ACTH and beta-LPH. We have reported that ASF is a true aldosterone secretagogue and readily distinguishable from ACTH, A II and beta-LPH. The present study suggests ASF shares a common rate-limiting final pathway of steroidogenesis, which may be the step between corticosterone to aldosterone, with ACTH, A II and beta-LPH.
In the perfused rat mesenteric vascular bed, the effects of magnesium and calcium on the vasoconstrictor responses to norepinephrine or potassium chloride were studied. Higher concentrations of magnesium in the perfusate attenuated the vascular responses to norepinephrine and potassium chloride in a dose-related manner. Higher concentrations of calcium in the perfusate enhanced greatly the vascular responses to potassium chloride, while the response to norepinephrine was only slightly potentiated by increasing calcium concentration. The attenuating effect of magnesium on the responses to norepinephrine and to potassium chloride were reversed by elevation of calcium concentration in the perfusate. The potentiating effects of calcium on the responses to potassium chloride were also reversed by increasing the concentration of magnesium. However, an inhibitory effect of magnesium on the responses to norepinephrine was not observed in the presence of higher concentrations of calcium. These results indicate that magnesium acts antagonistically on calcium movement in vascular contractions due to potassium chloride, but that the relationship between magnesium and calcium is more complex in vascular contractions induced by norepinephrine.
Of 103 borderline essential hypertensives below the age of 36 years, 11 (10.7%) showed low renin, 57 (55.4%) showed normal renin, and 35 (33.9%) showed high renin. Various hormones such as plasma catecholamines, PA, DOC, B, cortisol 18-OH-DOC, 18-OH-B, ACTH, AVP and PRL tended to be high in the high renin group and tended to be low in the low renin group. Furthermore, urinary excretion of kallikrein was also increased in the high renin group and reduced in the low renin group. There was no hormone which was increased in the low renin group. Regardless of renin levels, pressor responses to exogenous angiotensin II were increased in these juvenile essential hypertensives. From these studies on endocrine factors it is concluded that essential hypertensives are largely divided into 3 groups; the high hormone group, the normal hormone group and the low hormone group, and increased hormones may play an important role in the development of hypertension in the high hormone group. However, in the low hormone group and a part of the normal hormone group the mechanism of hypertension cannot be revealed by the study on endocrine factors.
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