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)

Measurements of blood plasma ACTH, hydrocortisone, STH, somatostatin, insulin, glucagon levels and plasma renin activity in 70 patients with borderline hypertension (BAH) and in 20 normal male subjects have revealed increased ACTH, hydrocortisone, and somatostatin levels, elevated plasma renin activity, and reduced STH and insulin levels in the patients. A possible role of the pressor hormone system activation in the pathogenesis of borderline arterial hypertension and in BAH transformation into essential hypertension is discussed.
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PMID:[Hormonal disorders in borderline arterial hypertension]. 257 58

Serum levels of 7 hormones and neuropeptides were studied in the course of development of a generalized epileptic activity (EA) induced in rats by intraperitoneal administration of corasole (75 mg/kg), i.e. 30 s (latent period), 50-150 s, 5-10 min after epileptogenic administration. A significant increase in the levels of ACTH (5.2-fold), glucagon (1.8.-fold), angiotensin I and renin activity were shown to occur 90-180 s later. Further on in the course of EA the level of ACTH remained enhanced but the level of glucagon and renin-angiotensin activity returned to normal. The levels of cortisol, vasopressin and aldosterone were enhanced 2-3-fold 30 min later. The level of insulin 30 min later remained unchanged. The role of neuropeptides and hormones in the onset and suppression of EA is discussed.
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PMID:[Changes in serum hormone and peptide levels in rats in experimental epilepsy]. 283 50

To clarify the role of the sympatho-adrenomedullary and renin-angiotensin-aldosterone systems, and catecholamine receptors, in the pathogenesis of orthostatic hypotension in diabetes mellitus (DM), urinary excretion of catecholamines, and plasma levels of norepinephrine (PNE), epinephrine (PE), renin activity (PRA), aldosterone (PAC), cyclic AMP (PcAMP) and cyclic GMP (PcGMP) were measured in 16 normal subjects (N) and 50 diabetic patients with or without orthostatic hypotension (DMOH(+), DMOH(-)). Changes in PNE, PE, PRA, PAC, PcAMP and PcGMP by standing, glucagon (G) administration and cold pressor test were examined. Furthermore, the effect of metoclopramide on catecholamine levels and blood pressure was investigated before and after cold pressor test. The results were following; (1) Urinary free norepinephrine excretion was significantly lower in DMOH(+), while urinary total norepinephrine excretion was normal in the two DM groups. Urinary free and total epinephrine excretions were lower in DMOH(+) than in N and DMOH(-). (2) PNE and PE were elevated after standing in all groups tested, and more pronounced in some cases of DMOH(+). Although PRA and PAC were elevated normally after standing in all groups, a dissociation between the two parameters was seen in some cases of DM. PcAMP after standing was correlated with PE(r = 0.829). Basal PcGMP was high in many cases of DMOH(+). However, no difference in the elevation of PcGMP after standing was noted between N and the two DM groups. (3) Systolic blood pressure (SBP) rose markedly in only DMOH(+) from 146 +/- 27mmHg to 178 +/- 34mmHg 5 minutes after G administration. The increment of PNE and PE 5 minutes after G administration were similar in all groups. In only DMOH(+), the increase in PcAMP 15 minutes after G test was proportional (r = 0.498) to that of epinephrine. (4) Responses of SBP, PNE, PE and PAC to cold pressor test apparently improved after administration of metoclopramide (MC) in some patients with DM. These results suggest that not only organic disturbance of sympathetic nerves but also functional inhibition of norepinephrine release mediated by dopamine receptor, may play an important role in the pathogenesis of orthostatic hypotension in diabetes mellitus. It is considered that catecholamine secretion from the adrenal medulla in DMOH(+) is increased by hypotension induced by standing. Furthermore, the vascular response to catecholamines may be accelerated through the increment of the extrajunctional receptor in DMOH(+).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The role of the sympatho-adrenomedullary system and adrenergic receptors in the pathogenesis of orthostatic hypotension in diabetes mellitus]. 285 93

1. The renal actions of ANP (average dose 30 ng kg-1 min-1 and glucagon (50 ng kg-1 min-1) were compared using fractional lithium reabsorption as the index of proximal reabsorption in groups of seven rats. Doses were chosen to cause similar increases in glomerular filtration rate (GFR). Time controls were included. 2. Glucagon raised GFR 32% and absolute proximal reabsorption (APR) 26% producing 81% effective proximal glomerulo-tubular balance (GTB) which was not significantly different from the 100% expected for perfect GTB. ANP raised GFR 33% and APR 10% indicating only 30% effective GTB (P less than 0.01). This was a significantly different effect from glucagon (P less than 0.005). 3. Sodium output increased 10-fold with ANP and 3-fold with glucagon. Filtration fraction increased 33% (P less than 0.04) above the pre-treatment value with ANP but was unchanged with glucagon. Plasma renin concentration was suppressed similarly by each hormone (46 and 36%, P less than 0.05, compared with pre-treatment values). 4. Despite a change in peritubular physical factors favouring reabsorption, there was almost complete attenuation of the increase expected in APR with the ANP-induced increase in GFR. In contrast, a similar change in GFR with glucagon resulted in an almost parallel increase in APR demonstrating maintenance of proximal GTB. 5. It is concluded that in the anaesthetized rat, ANP but not glucagon profoundly inhibits the increase in proximal reabsorption that normally follows an increase in filtered load. Such an action would contribute to the more potent natriuretic activity of ANP compared with glucagon.
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PMID:The effects of atrial natriuretic peptide and glucagon on proximal glomerulo-tubular balance in anaesthetized rats. 297 22

With the development of techniques for the qualitative and quantitative assessment of receptor function and knowledge of the biological responsiveness of neurotransmitter-mediated pathways, it is now quite clear that the response of a patient to a drug does not only involve the concentration of the drug in blood and tissue. Number and function of receptors are also important factors. A perturbation in which the receptor number is elevated is called "up-regulation", whereas "down-regulation" refers to the uncoupling between receptor and effector and the consecutive decrement in the receptor concentration. In general, there is an inverse relationship between the ambient concentration of the agonist and the number of its receptors and, therefore, the sensitivity of the target organ. The demarcation between alpha- and beta-adrenergic receptors has long been appreciated. Recent advances in the understanding of adrenergic receptors have led to the subdivision of beta-receptors; beta 1-adrenoceptors mediate the stimulation of rate and force of cardiac contraction and stimulate lipolysis. beta 2-adrenoceptors mediate smooth muscle relaxation and facilitate glycogenolysis and the release of insulin, glucagon and renin. The alpha-adrenergic receptors may also be divided into two subgroups. The alpha 1-adrenoceptors are postsynaptic located and facilitate smooth muscle constriction. Presynaptic located alpha 2-adrenoceptors mediate feedback inhibition of norepinephrine-release, while postsynaptic alpha 2-adrenoceptors facilitate smooth muscle contraction in selected vascular beds and stimulate the inhibition of various metabolic processes (insulin and renin secretion, lipolysis). The stage is now set for the application of the new knowledge of receptor function and regulation to the advancement of the practice of anaesthesia and intensive care.
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PMID:[Adrenoreceptors]. 298 84

A 5-year-old boy is described who presented with episodes of hypoglycaemia triggered by mild infections or fever. Subnormal glucocorticoid production was confirmed by demonstrating low urinary excretion of free cortisol, low plasma cortisol concentrations that did not rise after glucagon and ACTH stimulation, and by elevated plasma ACTH levels. The selective nature of the abnormality was confirmed by demonstrating normal plasma electrolyte concentrations and blood pressure on a salt-restricted diet. Plasma renin activity and plasma aldosterone levels were also normal and responded appropriately to salt restriction and to frusemide-induced diuresis. Starvation-induced hypoglycaemia was associated with raised levels of blood ketone bodies and low blood alanine concentrations. Catecholamine secretion during hypoglycaemia was reduced. Glucocorticoid replacement therapy was effective in restoring normal glucose homeostasis.
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PMID:Isolated glucocorticoid deficiency: metabolic and endocrine studies in a 5-year-old boy. 298 94

The effects of vitamin E (VE)-deficiency on renin release by various agents were examined using rat kidney cortical slices. Isoproterenol and glucagon in the presence or absence of theophylline increased renin release in the control group, while their stimulatory effects were attenuated by VE-deficiency. These decreased responses of renin release to isoproterenol and glucagon due to VE-deficiency were restored to the control level by dietary supplementation of dl-alpha-tocopheryl acetate or N,N'-diphenyl-p-phenylenediamine. The stimulatory effect of dibutyryl cyclic AMP or theophylline on renin release was not affected by VE-deficiency. These results suggest that in case of VE-deficiency, the response of renin release to stimuli is decreased via cyclic-AMP production.
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PMID:Renin release from kidney cortical slices in response to isoproterenol and glucagon is decreased in vitamin E-deficient rats. 299 73

To examine the relationship between prostaglandin E2 (PGE2) and renin release, glucagon, dopamine and dibutyryl cyclic AMP (DB-cAMP) were infused into dog kidneys during autoregulatory dilation of preglomerular vessels. Autoregulatory vasodilation, which enhances PGE2 and renin release, was induced by renal arterial constriction or ureteral occlusion. Glucagon infusion increased both PGE2 and renin release during autoregulatory vasodilation, and renin release was almost abolished after inhibiting PGE2 release by indomethacin. In contrast, dopamine and DB-cAMP infused during autoregulatory vasodilation increased renin release without significantly changing PGE2 release. Stimulation of renin release was not dependent on vasodilatory effects, which for all drugs were greatly diminished during autoregulatory vasodilation. Hence, glucagon stimulates both PGE2 and renin release. Most of the increase in renin release during glucagon infusion is prostaglandin-dependent since indomethacin greatly reduced the stimulatory effect. In contrast, dopamine and DB-cAMP stimulate renin release without increasing PGE2 release as previously found for beta-adrenergic stimulation.
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PMID:Dissociation between renal prostaglandin E2 and renin release. Effects of glucagon, dopamine and cyclic AMP in dogs. 300 5

In nine splenectomized male dogs a splenic artery, -splenic vein shunt was made. Before splenectomy and 3, 6 and 18 months after arterialization of portal blood, different metabolic and endocrine parameters were estimated. Long-term arterialization of portal blood was followed by only insignificant increase of portal vein pressure but a significant drop of pCO2 and increase of pO2 in portal blood was recorded. Simultaneously, a significant decrease of the erythrocyte count, hematocrit value, serum cholesterol and uric acid levels, and a shortening of the T1/2 of insulin and glucagon were found. In contrast, long-term arterialization of portal blood was followed by a significant increase of serum triglycerides, alpha2-globulins, plasma renin activity, cortisol, gastrin and 25-hydroxyvitamin D, and by slight carbohydrate intolerance. No morphological abnormalities in the liver and kidney tissue were found. Data presented in this paper suggest usefulness of a splenic artery-splenic vein shunt in the treatment of some metabolic disorders and of the failing hepatocytes.
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PMID:Metabolic effects of long-term arterialization of portal blood. 309 52

Although the existence of postprandial renal hyperemia and hyperfiltration has been established, the precise mechanism governing protein-mediated increases in renal hemodynamics is not, as yet, clearly defined. Investigative effort over the past decade has provided at least two plausible mechanisms playing an important role in renal hyperemia and hyperfiltration associated with ingestion of a protein-rich meal: 1) blood-borne vasoactive agents (e.g., pancreatic glucagon and/or hepatic glomerulopressin); and 2) intrarenal mechanisms (e.g., the tubuloglomerular feedback system). Data supporting each of these two candidate mechanisms are reviewed as are data supporting the importance of other factors such as renal prostanoids, the renin-angiotensin system, and renal cyclic nucleotides. It is anticipated that future investigative effort will be stimulated by our present knowledge of postprandial renal hemodynamics so that one day we not only will know the precise mechanisms governing postprandial renal hyperemia and hyperfiltration but, in addition, may gain valuable insight into the pathogenesis of chronic renal disease.
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PMID:Potential mechanisms mediating postprandial renal hyperemia and hyperfiltration. 327 87


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