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)

Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma potassium alterations in acute alkalosis. Respiratory and metabolic alkalosis were induced by hyperventilation and intravenous NaHCO3 or tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced alkalosis provoked decreases in plasma potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced alkalosis elicited an increase in plasma potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01). Hypokalemia in respiratory alkalosis was associated with a decrease in the plasma norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of epinephrine, insulin, glucagon, cortisol, and aldosterone. However, this hypokalemia was not affected by phentolamine. Also, somatostatin did not modify the hypokalemic response. NaHCO3-induced hypokalemia was associated with a decline in the plasma aldosterone and norepinephrine concentrations. The decline in plasma norepinephrine in NaHCO3-induced alkalosis followed the decrease in plasma potassium. In Tris-induced alkalosis, plasma insulin increased but norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma potassium alterations in bilaterally nephrectomized dogs with acute alkalosis.
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PMID:Role of hormonal factors in plasma K alterations in acute respiratory and metabolic alkalosis in dogs. 215 37

This paper discusses hormonal and metabolic reactions of healthy volunteers exposed to 14-day starvation. This exposure led to many-fold increase of plasma and urinary epinephrine (E); drastic increase of ACTH and beta-endorphin (BE), morning and integrated concentrations of cortisol and STH, aldosterone, T3, glucagon, cAMP, cGMP, cAMP-cGMP, acetyl choline (AC), free fatty acids (FFA), lactate, metanephrine (MN) excretion; decrease of plasma norepinephrine (NE) and unchanged NE excretion; decrease of plasma concentrations of TTH, T4, T3, prolactin (PL), insulin (morning and integrated concentrations), C-peptide, FSH, LH, testosterone, histamine, prostaglandins (PG) A + E, PG F2, glucose and pH, as well as decrease of excretion of homovanillic acid (HVA), vanillyl mandelic acid (VMA), normetanephrine (NMN) and MN-E, NMN:NE. On recovery day 14 concentrations of E, NE, BE, STH, AC, cAMP, cGMP, FFA as well as E and dopamine excretion remained elevated while concentrations of T3, PL, FT, LT, testosterone PG A + E, PG 2 and excretion of MN, HVA, VMA, MN:E remained decreased, while other parameters returned to the normal.
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PMID:[Hormonal and metabolic reactions in the human body during prolonged starvation]. 237 73

After burn trauma, a very marked endocrine response occurs. Almost all the known hormones take part in it. Their response influences very much the postburn metabolic changes and participates in the integration of the body's response with the nervous and immune systems. In this review, mainly the changes in various hormone levels are described, as well as the possible role of the acute phase response after burn trauma, and the communications between the endocrine and immune systems, the cells of the latter are able to respond to various hormonal stimuli and to secrete various hormones themselves. Some of the hormones are very sensitive indicators of the burn stress, e.g., the T3 levels (very low), testosterone in males (very low), dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) (very low), ADH, catecholamines, renin and angiotensin II, cortisol (high), 17-beta-estradiol in males (usually elevated). Other hormones are usually elevated, but not always (ACTH, aldosterone, prolactin, glucagon, immunoreactive insulin, beta-endorphin, rT3, 11-beta-hydroxyandrostenedione), but there are hormones that are unually low (T4, FSH, androstenedione, progesterone--the latter especially in females). Calcitonin, parathyroid hormone, growth hormone are sometimes elevated, as well as LH (measured with RIA methods). TSH is usually normal, the biologically measured LH was reported to be low. The levels of the sensitive indicators of burn stress may be used to evaluate the effect of treatment: if the burn patient is properly treated, the indicators may become earlier normal.
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PMID:Endocrine changes after burn trauma--a review. 251 73

Data presented in this study suggest existence of hyperendorphinism in uraemic patients. This hyperendorphinism may be regarded both as a primary beneficial compensatory mechanism counteracting disturbances of the internal environment, while causing secondary harmful side effects, which contribute to the uraemic state. Erythropoietin treatment of uraemic, haemodialyzed patients is followed by marked endocrine alterations (suppression of plasma levels of STH, ACTH, prolactin, glucagon, aldosterone, cortisol and plasma renin activity, elevation of plasma insulin and atrial natriuretic levels, lack of influence on plasma PTH, CT and AVP). It remains to be clarified whether the erythropoietin induced endocrine alterations are due to correction of the existing anaemia or reflect a specific effect of this hormone.
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PMID:Endocrine abnormalities in patients with endstage renal failure. 256 Mar 46

A hypotensive effect of an orally-administered cyclopeptide somatostatin analog, MK-678, has been demonstrated in a hypertensive diabetic rat model. Sustained blood pressure reduction failed to occur when the drug was administered to the spontaneously hypertensive rat. The mechanism of hypotension appears independent of effects on a variety of hormones including insulin, glucagon, growth hormone, and components of the renin-angiotensin system including renin activity, plasma angiotensin converting enzyme, and aldosterone.
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PMID:Blood pressure reduction in hypertensive-diabetic rats by the somatostatin analog MK-678. 256 53

We investigated the effects of sevoflurane anesthesia and of surgery, on the endocrine functions as reflected by plasma levels of cortisol, aldosterone, ACTH, beta-endorphin-like immunoreactivity, prolactin, insulin, growth hormone, glucagon and glucose in surgical patients.
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PMID:Endocrine evaluation of sevoflurane, a new inhalation anesthetic agent. 262 72

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

In a randomised controlled trial, preterm babies undergoing ligation of a patent ductus arteriosus were given nitrous oxide and d-tubocurarine, with (n = 8) or without (n = 8) the addition of fentanyl (10 micrograms/kg intravenously) to the anaesthetic regimen. Major hormonal responses to surgery, as indicated by changes in plasma adrenaline, noradrenaline, glucagon, aldosterone, corticosterone, 11-deoxycorticosterone, and 11-deoxycortisol levels, in the insulin/glucagon, molar ratio, and in blood glucose, lactate, and pyruvate concentrations were significantly greater in the non-fentanyl than in the fentanyl group. The urinary 3-methylhistidine/creatinine ratios were significantly greater in the non-fentanyl group on the second and third postoperative days. Compared with the fentanyl group, the non-fentanyl group had circulatory and metabolic complications postoperatively. The findings indicate that preterm babies mount a substantial stress response to surgery under anaesthesia with nitrous oxide and curare and that prevention of this response by fentanyl anaesthesia may be associated with an improved postoperative outcome.
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PMID:Randomised trial of fentanyl anaesthesia in preterm babies undergoing surgery: effects on the stress response. 2092 62

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


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