Effects of glucagon on the renal hemodynamics of dogs

Ueda, Juro; Nakanishi, Hironori; Miyazaki, Mizuo; Abe, Youichi

doi:10.1016/0014-2999(77)90210-2

Cited by 34 publications

(19 citation statements)

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“…In fact, glucagon increased GFR and adenosine decreased GFR significantly at normal pressure. Our results confirm the data obtained in previous in vivo studies (4,5,8,9,21,26). These GFR responses might be induced by the change in the glomerular filtration coefficient.…”

Section: Discussionsupporting

confidence: 91%

“…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). However, there is still no clear evidence concerning the intrarenal vascular sites of action of glucagon.…”

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confidence: 95%

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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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Section: Discussionsupporting

confidence: 91%

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confidence: 95%

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

Aki

Shoji

Hasui

et al. 1990

Japanese Journal of Pharmacology

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“…During the last decade, numerous studies have appeared describing the vasodilator effects of glucagon in the hepatic (Kock, Roding, Hahnloser, Richardson & Withrington, 1976 a,b;1977), mesenteric 1971;Ross, 1970;Ulano, Treat, Shanbour & Jacobson, 1972;MacFerran & Mailman, 1977) or renal (Stowe & Hook, 1970;Levy & Starr, 1972;Levy, 1975 a,b;Ueda, Nakanishi, Miyazaki & Abe, 1977) vascular beds of anaesthetized dogs or cats.…”

Section: Introductionmentioning

confidence: 99%

Studies on the Mechanism of Action of Glucagon in Strips of Rabbit Renal Artery

Gagnon

Regoli

Rioux

1980

British J Pharmacology

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The vasodilator effects of glucagon and adenosine cyclic 3′,5′‐monophosphate (cyclic AMP) were evaluated in strips of rabbit renal artery contracted with noradrenaline (NA) in the absence and presence of phosphodiesterase inhibitors or calcium (Ca2+) antagonists. The vascular relaxant effect of glucagon was markedly potentiated by various concentrations of four different phosphodiesterase inhibitors (papaverine, theophylline, 3‐isobutyl‐1‐methylxanthine (IBMX) and indomethacin), while that of cyclic AMP was potentiated by only two of them (papaverine and indomethacin) and inhibited by the others (theophylline and IBMX). Amongst the four phosphodiesterase inhibitors, IBMX (10 μg/ml) was found to produce the largest potentiation (e.g. the sensitivity increased by a factor of 10) of glucagon‐induced vascular relaxations (ED50 of glucagon in the presence of IBMX = 9.2 ± 1.0 ng/ml). Ca2+ antagonists such as verapamil and SKF 525A produced a dose‐dependent inhibition of the vasodilator action of glucagon. Verapamil (2.5 μg/ml) also antagonized cyclic AMP‐induced vascular relaxations. The vasodilator effect of verapamil was inhibited dose‐dependently by raising the concentration of extracellular Ca2+ from 0.05 to 0.2 g/l (or 1.25 to 5.0 mm) while those elicited by glucagon or cyclic AMP were not influenced, thus suggesting that the latter two drugs do not interfere with Ca2+ influx. Disodium edetate (Na2EDTA, 210 to 840 μg/l) produced a dose‐dependent vasodilator effect which was attributed to the facilitation of Ca2+ extrusion from the smooth muscle cells and/or Ca2+ binding to the cell membrane. The relaxation produced by Na2EDTA was significantly blocked by verapamil (10 μg/ml) or SKF 525A (10 μg/ml). The results were taken as an indication that glucagon produces at least a fraction of its vasodilator effect by promoting Ca2+ extrusion from the vascular smooth muscle cells and/or Ca2+ binding to or sequestration into intracellular sites, presumably via a cyclic AMP‐dependent mechanism.

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“…Glucagon infusion into either peripheral vein, portal vein or renal artery increases renal plasma flow, glomerular filtration rate and urine flow rate in animals with simple stomachs (Levy & Starr, 1972;Ueda, Nakanishi, Miyazaki & Abe, 1977;Premen, Hall & Smith, 1985;Aki et al 1990;Ahloulay, Bouby, Machet, Kubrusly, Coutad & Bankir, 1992). These effects could be explained in various ways.…”

Section: Introductionmentioning

confidence: 99%

“…These effects could be explained in various ways. Glucagon could induce vasodilatation of afferent arterioles (Ueda et al 1977) and gluconeogenesis in the proximal tubule with a subsequent change of water reabsorption in this nephron segment (de Rouffignac, Elalouf & Roinel, 1991). The well-known effect of glucagon on glomerular filtration rate in animals with simple stomachs might be due to an indirect action which stimulates a substance such as glomerulopressin from the liver (Uranga & Fuenzalida, 1975).…”

Section: Introductionmentioning

confidence: 99%

The renal response of sheep to intraportal infusion of glucagon

Faix¹,

Leng²

1997

Experimental Physiology

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SUMMARYThe effects on renal functions of infusing glucagon (100 ng kg-1 min-') into the portal vein system were studied in young anaesthetized sheep kept on a diet with normal protein and digestible energy contents. The clearance measurements of the left kidney functions showed a decreased urine flow rate (from 0(36 + 0.04 to 0 18 + 0(03 ml min-1; P < 0.01) within the first 1(0 min of glucagon infusion, f:alling to 007 + 002 ml min-' (P < 0.01) during the next 10 min. The glomerular filtration rate also decreased from 17 56 + 2 92 ml min-1 to its lowest value, 3 34 + 1.02 ml min-', (P < 0.01) after 20 min of glucagon infusion. Decreases in urea excretion (from 53.1 + 6-46 to 3-82 + 1 27 jumol min-'-P < 0 01) and osmotic clearance (from 0 67 + 0 13 to 0 09 + 0-02 ml min-1; P < 001) occurred during the first 20 min. The plasma level of glucose increased from 4(01 + 053 to 8 33 + 1 12 mmol 1-(P < 0.05) 20 min after the start of glucagon infusion. Twenty minutes after the start of glucagon infusion, the values of all the parameters measured began to recover, although they did not reach the control level, even after I h. Blood pressure was stable during the whole experiment. The results show that the effects of intrLaportally infused glucagon on kidney functions in sheep are the opposite of those obtained from similar experiments in laboratory animals with simple stomachs or in humans.

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Effects of glucagon on the renal hemodynamics of dogs

Cited by 34 publications

References 10 publications

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

Intrarenal Vascular Sites of Action of Adenosine and Glucagon

Studies on the Mechanism of Action of Glucagon in Strips of Rabbit Renal Artery

The renal response of sheep to intraportal infusion of glucagon

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