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  • Author: Shinpei Morimoto x
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Ryoyu Takeda, Shinpei Morimoto, Mitsuhiko Kuroda and Mototaka Murakami

ABSTRACT

A 23-year-old man with Marfan's syndrome (forme fruste) and renal tubular acidosis presented a syndrome closely resembling that reported by Bartter et al. (1962), i.c., a markedly increased plasma renin activity (PRA), hypokalaemia with normal blood pressure, decreased response of blood pressure to angiotensin II infusion and hyperaldosteronism. Hyperplasia of the juxtaglomerular apparatus was seen on renal biopsy. The studies on renal tubular function demonstrated that the patient had a unique feature corresponding to a proximal type of renal tubular acidosis (RTA).

During the period of sodium restriction the patient showed an abrupt decrease in sodium excretion to near or below intake levels with a tendency to potassium conservation but PRA remained unchanged. Sodiumloading did not suppress the increased level of PRA and albumin infusion showed only a little suppression of PRA. On the other hand, the oral administration of furosemide induced a significant increase in PRA. Replacement therapy with potassium induced a marked elevation of the urinary aldosterone level with a concomitant decrease in PRA when the serum potassium rose, but the PRA still remained above a level 10 times as high as the normal value.

These findings suggested that the mechanism of renin secretion in this patient was reset at a high level. A hypothetical role of PRA in the reset mechanism of renin secretion and pathophysiology of this patient are discussed. The relationship between RTA and Marfan's syndrome remains obscure.

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Sadahide Azukizawa, Ikuyo Iwasaki, Toshikazu Kigoshi, Kenzo Uchida and Shinpei Morimoto

Abstract. To evaluate the heparin effects in vivo and in vitro on adrenal angiotensin II receptors and angiotensin II-induced aldosterone production, we examined the angiotensin II binding and the maximum angiotensin II-induced aldosterone production using adrenal glomerulosa cells from rats treated with a heparin preparation containing benzyl alcohol (1500 IU/kg, twice daily for 6 weeks) or cells to which heparin (300 IU/l) was directly added. Comparison was made using the cells from rats treated with vehicle or the cells to which vehicle was directly added. Specific binding of [125I]iodo-angiotensin II was decreased in the cells from heparin-treated rats or in the heparin-treated cells. Scatchard analysis showed that the decrease in binding was due to a decrease in both the number and the affinity of angiotensin II receptors in the cells from heparin-treated rats and a decrease in the number, but not the affinity, of the receptors in the heparin-treated cells. Heparin also caused a decrease in the maximum angiotensin Il-induced production, but not the basal production, of aldosterone in the cells from heparin-treated rats and in the heparin-treated cells. These data suggest that heparin interacts with adrenal angiotensin II receptors to inhibit the angiotensin Il-induced aldosterone production.

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Ryoji Iwasaki, Toshikazu Kigoshi, Kenzo Uchida and Shinpei Morimoto

Abstract.

To examine the nature of adrenal abnormalities in diabetic patients with hyporeninemic and normoreninemic hypoaldosteronism, responses of plasma 18-hydroxycorticosterone and plasma aldosterone to angiotensin II infusions and ACTH injection were investigated in 8 diabetic patients with hyporeninemic hypoaldosteronism and 9 diabetic patients with normoreninemic hypoaldosteronism compared to 11 control subjects. In both the patients with hyporeninemic and normoreninemic hypoaldosteronism, plasma 18-hydroxycorticosterone and plasma aldosterone were low, whereas plasma cortisol and plasma corticosterone were within normal ranges. Percent increments of plasma 18-hydroxycorticosterone and plasma aldosterone above their baseline levels after angiotensin II infusions were low or somewhat low in the patients with hyporeninemic hypoaldosteronism and low in the patients with normoreninemic hypoaldosteronism. Percent increments of plasma 18-hydroxycorticosterone and plasma aldosterone above their baseline levels after ACTH injection were similar in the three groups. These results suggest that in diabetic patients with isolated hypoaldosteronism, the adrenal abnormality, regardless of whether it is primary or secondary, is mainly due to impaired adrenal responsiveness to angiotensin II and atrophy of the zona glomerulosa.

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Ryoyu Takeda, Shinpei Morimoto, Kenzo Uchida, Isamu Miyamori and Tetsuji Hashiba

Abstract.

The plasma aldosterone response to angiotensin II (10 ng/kg/min for 30 min, iv) under conditions of varied sodium intake was studied in 10 young subjects (20 to 35 years), 9 middle-aged (41 to 56 years) and 11 elderly (66 to 73 years) normotensive subjects. Basal plasma renin activity, basal plasma level and urinary excretion of aldosterone were significantly lower in the elderly than in the young and middle-aged groups on both 130 and 25 mEq sodium intakes. When sodium intake was reduced to 25 mEq for 3 days, the weight loss was significantly greater in the elderly than in the young and middle-aged groups. No significant differences in blood pressure and serum electrolytes were found between the three groups. Angiotensin II infusion caused significant increases in the mean blood pressure in all the three groups, but to a greater extent in the elderly group. Plasma aldosterone level and its absolute increment, but not its per cent increment, after angiotensin II infusion were significantly lower in the elderly than in the young and middle-aged groups. In combined young, middleaged and elderly subjects, the absolute plasma aldosterone increment correlated positively with basal plasma aldosterone and plasma renin activity levels on a 25 mEq sodium intake, and with plasma renin response to sodium restriction.

These results suggest that ageing may cause a lesser plasma aldosterone response to angiotensin II with a decrease in basal plasma aldosterone, in parallel with a decrease in plasma renin activity, under condition of low sodium diet.

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Ryoyu Takeda, Shinpei Morimoto, Kenzo Uchida and Isamu Miyamori

ABSTRACT

Changes in serum electrolytes, haematocrit, plasma renin activity and plasma aldosterone induced by glucose and insulin (GI) infusion were serially investigated in seven patients with periodic thyrotoxic paralysis. An attack which developed into complete quadriplegia was induced within 90 min after the beginning of the GI infusion in four out of seven patients. Only a slight paralysis of the legs was produced in another two patients and induction of an attack did not materialize in one. In four patients with complete quadriplegia, the mean values of serum sodium and potassium concentrations, haematocrit, plasma renin activity and plasma aldosterone slightly decreased immediately after the beginning of the GI infusion. Induction of a paralytic attack was not accompanied by any significant changes in serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone either 15 min before or after the onset of attack, while the serum potassium concentration progressively decreased, and an increase in plasma aldosterone associated with an increase of haematocrit and plasma renin activity reached a peak level at the stage of complete quadriplegia. On the other hand, in the three patients in whom an infusion produced slight or no paralysis of the legs, changes in the serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone were insignificant and the serum potassium concentration was slightly but insignificantly decreased.

These results suggest that hyperaldosteronism may not be a trigger for the induced paralytic attack but a phenomenon secondary to volume depletion and a change in potassium homoeostasis induced by GI infusion.

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Shigeru Nakano, Kenzo Uchida, Takashi Ishii, Mihoko Takeuchi, Sadahide Azukizawa, Toshikazu Kigoshi and Shinpei Morimoto

Nakano S, Uchida K, Ishii T, Takeuchi M, Azukizawa S, Kigoshi T, Morimoto S. Association of a nocturnal rise in plasma alpha-atrial natriuretic peptide and reversed diurnal blood pressure rhythm in hospitalized normotensive subjects with non-insulin dependent diabetes mellitus. Eur J Endocrinol 1994;131:184–90. ISSN 0804–4643

Diurnal changes in plasma atrial natriuretic peptide (ANP), plasma renin activity (PRA) and plasma aldosterone as related to those in blood pressure (BP) were studied under hospital conditions in 18 diabetic subjects without proteinuria and 8 age-matched control subjects. Of 18 diabetic subjects, 10 had a normal diurnal BP rhythm with the peak value in the afternoon (group 1) and 8 had a reversed BP rhythm with the peak value during the night (group 2). Autonomic dysfunction estimated by measuring orthostatic BP and heart-rate changes and beat-to-beat heart-rate variations was more pronounced in group 2 than in group 1. Fasting plasma glucose and HbA1c were similarly high in both diabetic groups. Group 1 showed modestly elevated mean 24-h MBP and plasma ANP levels, modestly low mean 24-h PRA and plasma aldosterone levels, and a lack of diurnal ANP changes similar to that in controls. Group 2 showed markedly elevated mean 24-h BP and plasma ANP levels, markedly low mean 24-h PRA and plasma aldosterone levels, and nocturnal rises in plasma ANP and BP. PRA and plasma aldosterone exhibited circadian rhythms with their peak values found in the early morning in all three groups. The daytime/overnight excretion ratios of sodium and water were normal in group 1 and low in group 2. These results indicate that diurnal changes in plasma ANP, PRA and plasma aldosterone are altered in diabetic subjects with normal and reversed diurnal BP rhythms, predominantly in the latter.

Shigeru Nakano, Division of Endocrinology, Department of Internal Medicine, Kanazawa Medical University, 1-1 Daigaku, Uchinada, Ishikawa 920-02, Japan