Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two Holstein bull calves each were infused intravenously with 1 mg glucagon in .9% sodium chloride, and two were given saline alone; 1 wk later treatments were reversed. Glucagon increased concentrations of insulin and glucose but decreased potassium in blood plasma and moderately increased urinary magnesium and calcium losses. When only saline was used, there was no effect. A hypothesis relating elevated glucagon to grass tetany is proposed.
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PMID:Effect of glucagon infusion on plasma magnesium, glucose, and insulin in bull calves. 96 39

In a previous communication we demonstrated that pentagastrin-induced gastric acid secretion is strongly and equally inhibited by intrajejunal infusions of hypertonic glucose, hypertonic sodium chloride, and triglycerides. Samples of peripheral venous blood obtained during these experiments were now analysed for insulin, glucose, pancreatic glucagon, and enteroglucagon. Pancreatic glucagon was stimulated weakly only by triglycerides. Enteroglucagon secretion was strongly stimulated by glucose, moderately by triglycerides, and unaltered after sodium chloride. Insulin secretion was stimulated only during the glucose infusion. We concluded that enteroglucagon is not responsible for the jejunal inhibition of gastric acid secretion in man by jejunal administration of hyperosmolal NaCl solution but may participate in the inhbition evoked by jejunal administration of glucose of triglycerides. Furthermore, it is unlikely that enteroglucagon is in itself insulinogenic in man.
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PMID:The enteroglucagon response to intrajejunal infusion of glucose, triglycerides, and sodium chloride, and its relation to jejunal inhibition of gastric acid secretion in man. 127 5

The effects of an adenosine analog, N6-phenyl-isopropyl-adenosine (PIA), on the glucagon-stimulated adenylate cyclase activity in rat hepatic membranes were studied. Adenosine at high concentrations (greater than 10 microM) has been reported exclusively to inhibit the adenylate cyclase via intracellular P-sites of the hepatic membrane. The stimulation by glucagon of the enzyme was attenuated by nanomolar concentrations of PIA in the presence of low concentrations (less than 1.0 microM) of GTP, indicating the effect of the guanine nucleotide inhibitory system (Ni). This inhibition by PIA required the presence of sodium chloride and was antagonized with isobutyl methylxanthine, an antagonist for the extracellular R-site receptors. The inhibitory effects of PIA disappeared and reversed into a stimulatory phase with increasing concentrations of GTP, suggesting the presence of a stimulatory (Ns) and an inhibitory (Ni) guanine nucleotide system of the enzyme in the action of the adenosine. PIA concentrations over a micromolar were observed to stimulate the enzyme activity in a GTP-dependent manner, indicating the presence of the stimulatory receptor (A2 or Ra) coupled to the Ns. These results suggest that receptors for adenosine of the inhibitory type (A1 or Ri) and the stimulatory type (A2 or Ra) are present on the rat hepatic membrane, showing multiple controls of the adenylate cyclase system, depending on the cellular concentrations of GTP and/or sodium chloride.
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PMID:Multiple controls by adenosine receptors on the adenylate cyclase in the rat hepatic membrane. 169 17

The effect of cyclic somatostatin on early and late dumping syndrome was studied in 12 patients with gastric resection. Each patient underwent two glucose challenges with 75 grams of glucose administered orally. In the control study isotonic sodium chloride was given, while in the other study cyclic somatostatin in a dose of 250 micrograms bolus injection followed by infusion of 80 ng/kg/min for a period of 270 minutes. In the control study all patients showed subjective symptoms of the early dumping syndrome with significant increases in pulse rate, hematocrit, and vasoactive intestinal polypeptide. Ten patients showed asymptomatic hypoglycemia, as a sign of the late dumping syndrome associated with a significant increases of insulin, gastric inhibitory peptide and glucagon levels. During the administration of somatostatin these changes failed to develop. These results indicate that somatostatin alleviates the symptoms of early and late postprandial dumping syndrome.
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PMID:[The effect of somatostatin in dumping syndrome]. 197 48

1. Plasma levels of atrial natriuretic peptide and several other hormones were measured and related to the renal responses to chronic changes in the dietary intake of protein and sodium, alone and in combination. Eight healthy subjects consumed four diets for 1 week: a basal diet containing 140 mmol of sodium/day and 1 g of protein day-1 kg-1, the same diet with isocaloric addition of 1 g of meat protein day-1 kg-1, the basal diet with addition of 170 mmol of sodium chloride/day and the basal diet with both additions. 2. Creatinine clearance was increased significantly both by protein and, to a smaller extent, by sodium. Plasma atrial natriuretic peptide and the urinary excretion of guanosine 3':5'-cyclic monophosphate were increased significantly by sodium but were not affected by protein. Protein induced a significant rise in plasma glucagon levels, whereas the rise in somatomedin C (insulin-like growth factor I) just failed to reach statistical significance. 3. These findings demonstrate that atrial natriuretic peptide does not mediate chronic protein-induced hyperfiltration, although it may contribute to the renal effects of sodium. Glucagon and somatomedin C (insulin-like growth factor I) may have contributed to chronic protein-induced hyperfiltration.
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PMID:Atrial natriuretic peptide and chronic renal effects of changes in dietary protein and sodium intake in man. 216 88

In order to know the role of cytosolic calcium in the modulation of the hormone action on sodium chloride transport across the thick ascending limbs of Henle's loop, we examined whether verapamil, a blocker of cellular calcium entry, can modulate the effects of arginine vasopressin (AVP) or glucagon in stimulating transepithelial voltage (Vt) and cyclic AMP generation in the mouse medullary thick ascending limb (MAL). The pretreatment of the renal tubule with 5 X 10(-5)M verapamil reduced the Vt stimulated with 200 microU/mliter AVP from 1.7 +/- 0.3 mV to 0.4 +/- 0.4 mV (N = 7, P less than 0.05). The changes in Vt were well correlated with those of unidirectional Cl flux from the lumen to the bath. However, verapamil did not influence the Vt stimulated with 10(-3) M dibutyryl cyclic AMP. The pretreatment of the MAL with 10(-5) M verapamil also inhibited the cyclic AMP generation in the MAL from 72.1 +/- 17.9 to 50.6 +/- 13.6 fmoles/mm/7 min (N = 7, P less than 0.05) as well as in the medullary collecting tubule from 147.6 +/- 46.6 to 121.2 +/- 41.6 fmoles/mm/7 min (N = 4, P less than 0.05). The effect of verapamil in inhibiting the AVP-stimulated cAMP was dose-dependent: the cAMP generation was inhibited by 28.9 +/- 6.8 and 61.1 +/- 9.3% with 10(-5) M and 10(-4) M verapamil, respectively. When verapamil was added to the medium simultaneously with AVP, the generation of cyclic AMP was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation by verapamil of hormonal action on the Henle's loop of mice. 242 41

The impact on renal sodium chloride reabsorption of an acute increase in glomerular filtration rate (GFR) induced by atrial natriuretic factor (ANF) or glucagon was examined in the conscious rat. These hormones have no direct effect on proximal solute transport and have opposite effects on distal transport. ANF and glucagon increased GFR to a comparable extent (2.0 +/- 0.2 to 3.5 +/- 0.4 ml/min, p less than 0.01, and 1.9 +/- 0.1 to 3.3 +/- 0.1 ml/min, p less than 0.001, respectively). While most (95-97%) of the increment in filtered sodium chloride was reabsorbed, a small portion (3-5%) escaped tubular reabsorption. Absolute sodium and chloride urinary excretion rates increased similarly in response to each hormone, by two- to three-fold. Slightly imperfect load-dependent sodium chloride reabsorptive response by the nephron, despite opposite direct effects on distal nephron transport, may account for the observed natriuresis and chloruresis associated with the acute glomerular hyperfiltration induced by ANF or glucagon administration.
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PMID:Comparison of the natriuresis and chloruresis associated with glomerular hyperfiltration induced by atrial natriuretic factor or glucagon. 295 76

Acute fulminant hepatitis was induced in 55 healthy adult male rabbits with the potent hepatotoxin galactosamine hydrochloride (3.75 mmoles per kg i.v.). Control rabbits (n = 27) were divided into three groups: Group I (n = 10) underwent sham surgery for placement of an indwelling central venous catheter; Group II (n = 9) received 5% dextrose and water via an indwelling central venous catheter, and Group III (n = 8) received daily intramuscular injections of 0.9% sodium chloride. Treated rabbits (n = 28) also consisted of three groups: Group IV (n = 9) received 12-hr intravenous infusions of insulin (0.029 units per kg per hr) and glucagon (2.86 micrograms per kg per hr) daily; Group V (n = 10) received a continuous infusion of parenteral amino acids (Travasol), and Group VI (n = 9) received daily intramuscular methylprednisolone (0.69 mg per kg). In each case, treatment was initiated 16 hr following galactosamine injection. Serum aminotransferase activity was determined on Days 0, 1, 4 and 10 of the 10-day study. Liver histology was obtained immediately after death and graded under code on a scale of 1 to 4 for severity of hepatitis. Rabbits surviving 10 days were sacrificed on Day 10 for histologic examination. The extent of galactosamine-induced hepatic injury was similar in all six groups as manifest by peak mean SGPT (range: 2,662 to 3,568 IU per liter), SGOT (range: 4,435 to 5,625 IU per liter) levels and hepatic histologic findings. The overall survival rate in controls was 6/27 (22%); in insulin/glucagon-treated animals 2/9 (22%), and in the amino acid-treated group 2/10 (20%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparative study of the effects of insulin/glucagon infusions, parenteral amino acids and high dose corticosteroids on survival in a rabbit model of acute fulminant hepatitis. 351 Sep 52

Present evidence suggests that the renal handling of magnesium is normally a filtration-reabsorption process as evidence for secretion is unsubstantiated. Magnesium reabsorption has distinctive features when compared with that of sodium and calcium. The proximal tubule concentration of magnesium rises to levels about 1.5 times greater than the glomerular filtrate and only 20-30% of the filtered magnesium is reabsorbed in this segment. Although the fractional reabsorption of magnesium is only half that of sodium, it changes in parallel with that of sodium in response to changes in extracellular fluid volume. The major portion of filtered magnesium (some 65%) is reabsorbed in the loop of Henle and evidence indicates that the thick ascending limb is the principal segment involved in magnesium absorption. Recent observations suggests that magnesium reabsorption in the ascending limb may be voltage dependent and secondary to active sodium chloride reabsorption. The loop of Henle appears to be the major nephron site where magnesium reabsorption is regulated possibly by cAMP-mediated hormones including parathyroid hormones, calcitonin, glucagon and antidiuretic hormone. About 10% of the filtered magnesium is delivered into the distal nephron. The distal tubule reabsorbs only a small fraction of the filtered magnesium which may be regulated by the same cAMP-mediated hormones involved in control of magnesium in the loop.
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PMID:The physiology of renal magnesium handling. 354 6

To examine whether plasma growth hormone is necessary for the amino acid-induced rise in effective renal plasma flow (ERPF, PAH clearance) and GFR (inulin clearance), arginine HCl, 500 mg/kg, was infused for 30 minutes into eight normal and six growth hormone-deficient individuals. During infusion, ERPF increased in the normal and growth hormone-deficient subjects by 28.9 +/- 11.4 SD-% (P less than 0.01) and 46.5 +/- 14.4% (P less than 0.001). GFR rose by 23.7 +/- 5.9% (P less than 0.05) and 42.7 +/- 29.1% (P less than 0.001) in the two groups. Plasma growth hormone rose only in the normal subjects, while glucagon increased in both groups. Infusion of arginine HCl, 200 mg/kg, into normals increased ERPF and GFR without increasing plasma osmolality. Lower arginine doses essentially did not affect ERPF, GFR, growth hormone, or glucagon. Infusion of D-glucose into normals raised plasma osmolality as high as with arginine HCl, 500 mg/kg, but increased ERPF only slightly and not GFR; D-glucose infusion caused a delayed rise in growth hormone that was unassociated with an increase in ERPF or GFR. An infusion of ammonium chloride with sodium chloride, which provided an amount of chloride similar to the 500 mg/kg arginine HCl dose, did not change ERPF and GFR; this suggests that the chloride load did not cause the altered renal hemodynamics stimulated by arginine HCl. These findings indicate that neither normal plasma growth hormone levels nor a rise in growth hormone mediates the arginine-induced acute increase in ERPF or GFR. This effect is also not due to the osmolar load but could be caused by the rise in plasma glucagon.
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PMID:Role of growth hormone in the amino acid-induced acute rise in renal function in man. 366 97


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