Control by insulin of sodium potassium and water excretion by the isolated dog kidney

Nizet, A; Lefèbvre, Pierre; Crabbé, J.

doi:10.1007/bf00586561

Cited by 129 publications

(57 citation statements)

References 26 publications

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“…In addition, diuretic and natriuretic effects of a physiologic dose of insulin (i.v.) were not observed in our clearance experiments with fasted intact rats (unpublished data), and such findings are compatible with reports in humans and dogs (9,10). Therefore, the apparent natriuretic effect of insulin in intact rats (Fig.…”

Section: Discussionsupporting

confidence: 93%

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Natriuresis of Fasting in Intact and Adrenalectomized Rats

Nohno

Hayashi

Murayama

1977

Japanese Journal of Pharmacology

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Abstract-Experimentswere carried out in an attempt to elucidate the mechanism of fasting-induced natriuresis in conscious rats. Female animals were given a low sodium diet and saline in a fixed concentration for at least three days, and deprived of food thereafter. The sodium balance significantly shifted to negative independently of potassium supply in intact rats. Such was also observed in the dexamethasone replaced, adrenalectomized rats and was not affected by further administration of aldosterone.In addition, the diuretic effect of insulin in fasted intact rats was not evident in the fed diabetic rats in which diabetes had been induced by streptozotocin. Such findings suggested participation of factors other than insulin. The natriuresis of fasting in intact rats appears to involve two factors, one of which is independent of the sodium intake level. Dependence on the sodium intake level may be derived from alteration of the solute diuresis-like effect of drinking saline when animals are fasted. These results suggest that neither aldosterone nor insulin is a major causal factor involved in fasting-induced natriuresis.In man and rabbit, many workers have shown that fasting produced natriuresis, and such was arrested by carbohydrate feeding (1-8). Previous reports indicated that in rats also, food deprivation resulted in an increase in sodium excretion or a negative shift of sodium balance. Several hormones regulating the glucose metabolism may be involved in the occurrence of sodium imbalance during the early stage of fasting, however the mecha nism remains obscure.The antidiuretic effect of insulin (9, 10) has been attributed to fasting-induced natriuresis and anti -natriuresis by subsequent glucose feeding. In a preliminary report from this laboratory it was confirmed that the negative balance of sodium in fasted rats was not improved but rather enhanced by the administration of insulin (11). Since glucagon has a natriuretic effect in man and the dog (12)(13)(14), it is suggested that glucagon may contribute either directly or indirectly to the natriuretic effect of fasting. Moreover, well-known factors, such as aldosterone and antidiuretic hormone, may be implicated in the sodium imbalance.The present series of studies on the fasting-produced natruiresis was undertaken to determine: (a) The role of sodium and potassium loading in intact fasting rats; (b) the effect of aldosterone in glucocorticoid-replaced adrenalectomized rats; and (c) the effect of insulin in intact or diabetic rats. MATERIALS AND METHODSFemale Wistar rats weighing between 190 and 310 g were maintained on a regular diet

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Section: Discussionsupporting

confidence: 93%

“…The antidiuretic effect of insulin (9,10) has been attributed to fasting-induced natriuresis and anti -natriuresis by subsequent glucose feeding. In a preliminary report from this laboratory it was confirmed that the negative balance of sodium in fasted rats was not improved but rather enhanced by the administration of insulin (11).…”

mentioning

confidence: 99%

Natriuresis of Fasting in Intact and Adrenalectomized Rats

Nohno

Hayashi

Murayama

1977

Japanese Journal of Pharmacology

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“…At physiological concentrations, insulin increases sodium reabsorption in the isolated perfused kidney [6] without affecting renal haemodynamics or glomerular filtration rate. The exact site of tubular action of insulin is still unclear.…”

Section: Discussionmentioning

confidence: 98%

“…[Diabetologia (1997) 40: 770-777] Keywords Angiotensin II, autoradiography, captopril, insulin receptors, mRNA. 8], without affecting renal haemodynamics or glomerular filtration rate [6,9]. Recent experiments have shown that, in normal rats, there is an inverse relationship between dietary sodium intake and renal insulin receptor density and mRNA levels [10], suggesting the existence of a feedback mechanism that limits insulin-induced sodium retention when extracellular fluid volume is expanded.…”

Section: Discussionmentioning

confidence: 99%

“…When considering possible pathogenetic mechanisms that could mediate the prohypertensive effect of insulin, particular attention has been paid to the renal actions of the hormone. Insulin decreases urinary sodium excretion in rats [4], dogs [5,6], and humans [7, Diabetologia (1997) Summary Both the density and level of mRNA encoding insulin receptors in the kidney are inversely related to the dietary sodium content, suggesting a feedback mechanism that limits the insulin-induced sodium retention when extracellular fluid volume is expanded. Because angiotensin II affects tissue sensitivity to insulin in humans, we investigated whether angiotensin II affects insulin receptor binding and mRNA levels in the kidney, liver, and renal arteries of normal rats and rats with streptozotocin-induced diabetes mellitus.…”

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Effects of angiotensin II on insulin receptor binding and mRNA levels in normal and diabetic rats

et al. 1997

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The observation that hyperinsulinaemia and insulin resistance are present in subjects with essential hypertension has led to the hypothesis that insulin is involved in the pathophysiology of this disease [1][2][3]. When considering possible pathogenetic mechanisms that could mediate the prohypertensive effect of insulin, particular attention has been paid to the renal actions of the hormone. Insulin decreases urinary sodium excretion in rats [4], dogs [5,6], and humans [7, Diabetologia (1997) Summary Both the density and level of mRNA encoding insulin receptors in the kidney are inversely related to the dietary sodium content, suggesting a feedback mechanism that limits the insulin-induced sodium retention when extracellular fluid volume is expanded. Because angiotensin II affects tissue sensitivity to insulin in humans, we investigated whether angiotensin II affects insulin receptor binding and mRNA levels in the kidney, liver, and renal arteries of normal rats and rats with streptozotocin-induced diabetes mellitus. Non-diabetic and diabetic rats were infused for 7 days with either vehicle or angiotensin II at a rate of 200 ng ⋅ kg −1 ⋅ min −1 . In a separate experiment, normal rats were treated with an angiotensin converting enzyme inhibitor (captopril, 100 mg/dl in the drinking water) or vehicle for 7 days. Regional analysis of insulin receptor binding in the kidney and renal arteries was performed by an in situ technique using computerized microdensitometry and emulsion autoradiography. Insulin receptor mRNA levels were determined in renal and hepatic tissue by Northern blot hybridization and normalized with 28S rRNA. No differences in blood pressure were observed among diabetic and non-diabetic rats infused with either vehicle or angiotensin II, whereas captopril-treated rats had significantly lower blood pressure levels than their respective controls. Angiotensin II significantly decreased plasma renin concentration in both non-diabetic and diabetic rats. Insulin receptor number was significantly greater in the renal cortex of diabetic rats than in non-diabetics, whereas no significant differences were found in the outer medulla, inner medulla, or renal arteries. Angiotensin II infusion did not affect either the number or affinity of insulin receptors in any of the renal regions studied. Insulin receptor mRNA levels were significantly greater in the kidney and liver of diabetic rats than in non-diabetics and were not affected by angiotensin II infusion. Similar to angiotensin II infusion, captopril treatment did not affect either renal insulin receptor binding or mRNA levels. Thus, diabetic rats have increased insulin receptor binding and mRNA levels in comparison to non-diabetic rats. Angiotensin II infusion and captopril treatment do not affect insulin receptor binding and mRNA levels in the kidney, arguing against a role for this peptide in the modulation of renal sensitivity to insulin. [Diabetologia (1997) 40: 770-777]

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