Direct effects of glucagon on renal hemodynamics and excretion of inorganic ions

Pullman, Theodore N.; Lavender, A. R.; Aho, Impi

doi:10.1016/0026-0495(67)90047-9

Cited by 101 publications

(35 citation statements)

References 18 publications

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“…It has been reported that glucagon en hanced the urinary excretion of sodium and water (12)(13)(14), and when we infused glucagon into the renal artery in non-fasted rats a similar effect was noted (unpublished data). It was also reported that the plasma concentration of glucagon increased early in the fast (14,29,30).…”

Section: Discussionsupporting

confidence: 76%

“…6) has to be explained in terms of association of factor(s) other than insulin. For the decrease in ex cretion of sodium and water on days I and 2 of insulin therapy in diabetic rats, two factors may be responsible: (a) Disappearance of the solute diuresis-like effect of hyperglycemia with insulin therapy; (b) reduction of the natriuresis induced by glucagon (12)(13)(14) due to the restoration of insulin-deficient hyperglucagonemia by exogenous insulin (27,28).…”

Section: Discussionmentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

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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: 76%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Natriuresis of Fasting in Intact and Adrenalectomized Rats

Nohno

Hayashi

Murayama

1977

Japanese Journal of Pharmacology

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“…Several previous studies have shown that glucagon exerts natriuretic and phosphaturic effects (5,(47)(48)(49)(50)(51) by reducing the reabsorption of sodium, phosphate, and water in the whole proximal tubule, with a predominant influence in the pars recta (52). However, no glucagon receptors (53) and no glucagon-sensitive adenylate cyclase activity (54) have been found in this nephron segment.…”

Section: Groups Plasma Urea (Mm)mentioning

confidence: 75%

Cyclic AMP is a hepatorenal link influencing natriuresis and contributing to glucagon-induced hyperfiltration in rats.

Ahloulay¹,

Déchaux²,

Hassler³

et al. 1996

J. Clin. Invest.

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The effects of glucagon (G) on proximal tubule reabsorption (PTR) and GFR seem to depend on a prior action of this hormone on the liver resulting in the liberation of a mediator and/or of a compound derived from amino acid metabolism. This study investigates in anesthetized rats the possible contribution of cAMP and urea, alone and in combination with a low dose of G, on phosphate excretion (known to depend mostly on PTR) and GFR. After a 60-min control period, cAMP (5 nmol/min ϫ 100 grams of body weight [BW]) or urea (2.5 mol/min ϫ 100 grams BW) was infused intravenously for 200 min with or without G (1.2 ng/min ϫ 100 grams BW, a physiological dose which, alone, does not influence PTR or GFR). cAMP increased markedly the excretion of phosphate and sodium ( ϩ 303 and ϩ 221%, respectively, P Ͻ 0.01 for each) but did not alter GFR. Coinfusion of cAMP and G induced the same tubular effects but also induced a 20% rise in GFR ( P Ͻ 0.05). Infusion of urea, with or without G, did not induce significant effects on PTR or GFR. After G infusion at increasing doses, the increase in fractional excretion of phosphate was correlated with a simultaneous rise in plasma cAMP concentration and reached a maximum for doubling of plasma cAMP. These results suggest that cAMP, normally released by the liver into the blood under the action of G, ( a ) is probably an essential hepatorenal link regulating the intensity of PTR, and ( b ) contributes, in conjunction with specific effects of G on the nephron, to the regulation of GFR. ( J. Clin. Invest. 1996. 98: 2251-2258.)

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“…In the kidney, glucagon affects renal glomerular filtration, renal blood flow, and decreases renal tubular sodium reabsorption (Pullman et al, 1967). Part of the acute natriuretic action of glucagon are mediated by inhibition of NHE3 in the renal proximal tubule via a cAMP/PKAdependent pathway.…”

Section: Glucagonmentioning

confidence: 99%