Postprandial regulation of renal hemodynamics: role of pancreatic glucagon

Premen, A. J.; Hall, Jennifer.; Smith, M. J.

doi:10.1152/ajprenal.1985.248.5.f656

Cited by 54 publications

(49 citation statements)

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“…9,25 Glucagon is believed to be responsible for increased GFR after a high-protein meal or the glomerular hyperfiltration seen in early stages of diabetes. 10 Although MCs may, therefore, represent a major target of glucagon in the glomerulus, it remains unclear whether glucagon has a direct effect on MCs or the signaling mechanism(s) involved. The present study provides evidence that MCs express functional glucagon receptors.…”

Section: Discussionmentioning

confidence: 99%

Glucagon Receptor–Mediated Extracellular Signal–Regulated Kinase 1/2 Phosphorylation in Rat Mesangial Cells

Carretero

Shao

et al. 2006

Hypertension

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Abstract-Glucagon, a major insulin counterregulatory hormone, binds to specific G s protein-coupled receptors to activate glycogenolytic and gluconeogenic pathways, causing blood glucose levels to increase. Inappropriate increases in serum glucagon play a critical role in the development of insulin resistance and target organ damage in type 2 diabetes. We tested the hypotheses that: (1) glucagon induces proliferation of rat glomerular mesangial cells through glucagon receptor-activated phosphorylation of mitogen-activated protein kinase extracellular signal-regulated kinase 1/2 (p-ERK 1/2); and (2)

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Section: Discussionmentioning

confidence: 99%

Glucagon Receptor–Mediated Extracellular Signal–Regulated Kinase 1/2 Phosphorylation in Rat Mesangial Cells

Carretero

Shao

et al. 2006

Hypertension

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“…Thus, there is still no consensus as to the intrarenal vascular sites of action of adenosine. Glu cagon has also been noted as an endogenous regulator of renal hemodynamics, especially at the postprandial state (7). We reported that intrarenal administration of glucagon in creased RBF and GFR proportionally, in dicating the preferential dilation of the afferent arteriole (8,9).…”

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confidence: 81%

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

Aki

Shoji

Hasui

et al. 1990

Japanese Journal of Pharmacology

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Abstract-Our purpose was to localize the intrarenal vascular sites of action of adenosine and glucagon. Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured in anesthetized dogs, and renal perfusion pressure (RPP) was varied by an adjustable aortic clamp. At normal RPP, RBF was increased by all agents. In contrast, GFR was increased by glucagon, decreased by adenosine and unchanged by acetylcholine (ACh) or adenosine plus glucagon. The increases in RBF by glucagon occurred only at RPPs within the autoregulatory pressure range, and renal autoregulatory capability was attenuated during the infusion of glucagon. In contrast, adenosine increased RBF at RPPs both within and below the autoregulatory pressure range, and the autoregulatory capability was not perceptibly impaired. Superimposition of glucagon to adenosine caused further vasodilation, and the autoregulatory efficiency was completely attenuated. There was no difference between the RPP-RBF or RPP-GFR relations obtained during infusion of adenosine plus glucagon and ACh, which dilates both the afferent and efferent arterioles. It is generally accepted that afferent arteriolar resistance attains a minimum value at RPP near the lower limit of the autoregulatory range. Thus, our data indicate that glucagon and adenosine preferentially dilate the afferent arteriole and the efferent arteriole, respectively.

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“…Several studies have established that this hormone participates in, or is even indispensable for, the postprandial increase in GFR (6)(7)(8)(9)(10)(11). However, this effect of glucagon is probably indirect and involves other mediators (12) because the plasma concentration of glucagon required to increase GFR exceeds the usual peripheral concentration seen after a protein meal (6,10,13). Moreover, direct infusion of glucagon into the renal artery fails to increase GFR in dogs (10,14), humans (8), and rats (Ahloulay, M., personal observation).…”

Section: Introductionmentioning

confidence: 99%

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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Postprandial regulation of renal hemodynamics: role of pancreatic glucagon

Cited by 54 publications

References 0 publications

Glucagon Receptor–Mediated Extracellular Signal–Regulated Kinase 1/2 Phosphorylation in Rat Mesangial Cells

Glucagon Receptor–Mediated Extracellular Signal–Regulated Kinase 1/2 Phosphorylation in Rat Mesangial Cells

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

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

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