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)

1. Chlorothiazide twice a day plus atenolol, metoprolol, pindolol and propranolol in single daily doses administered to patients with essential hypertension achieved effective control of blood pressure. 2. Each beta-adrenoreceptor-blocking drug was associated with small, but significant, increases in plasma triglyceride concentrations and suppression of fasting immuno-reactive glucagon concentrations.
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PMID:beta-Adrenoreceptor-blocking agents and lipid metabolism. 3 7

The hemodynamic changes observed in patients with the "hyperkinetic" form of borderline (labile) essential hypertension (BEH) could be related to the hyperresponsiveness of cardiac beta-adrenergic receptors to catecholamines. The isoproterenol-induced increase in plasma cyclic adenosine 3':5'-monophosphate (cAMP) reflects the response of adenylate cyclase to beta-adrenergic stimulation, whereas a non-beta-receptor-mediated increase occurs with the administration of glucagon. Both substances were infused into 13 control subjects and 14 patients with the hyperkinetic form of BEH before and after propranolol administration. Baseline plasma cAMP concentrations were comparable in both groups. After 30 minutes of isoproterenol infusion (20 ng/kg per min) a significantly higher increase in plasma cAMP and heart rate and a smaller decrease in diastolic blood pressure were seen in this type of BEH than in control subjects. The increase in plasma cAMP and in heart rate correlated positively when all subjects were considered together. Propranolol abolished hemodynamic and humoral responses to a similar degree in both groups. The plasma cAMP responses to glucagon (200 ng/kg per min) were slightly lower in our patients with BEH than in control subjects and were not suppressed by propranolol. The data are compatible with a hyperreactivity of the beta-adrenergic receptors or of the adenylate cyclase or both in hyperkinetic BEH and could correspond to the previously observed exaggerated beta-adrenergic drive to the heart in this type of hypertension. The non-beta-receptor-mediated rise in plasma cAMP (glucagon), however, remains comparable in control subjects and BEH.
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PMID:Plasma cyclic adenosine 3':5'-monophosphate response to isoproterenol and glucagon in hyperkinetic borderline (labile) hypertension. 17 67

The effect of the calcium antagonist nicardipine on insulin secretion and glucose homoeostasis was investigated in elderly hypertensives with and without diabetes mellitus; 15 patients with essential hypertension for at least 10 years and normal glucose tolerance according to standard criteria (Group I) and 15 elderly hypertensive patients affected by Type 2 diabetes mellitus and on treatment with diet or oral drugs (Group 2). In the basal state, all patients were submitted to an oral glucose tolerance test (OGTT, 75 g) and an iv arginine test (30 g), on two different days and in random order. The same tests were repeated after one month of treatment with nicardipine 60 mg/day, in three spaced doses, the last being given 1 h before the post-treatment test. Nicardipine did not change overall glucose homoestasis, as assessed by haemoglobin Alc and fructosamine, nor did it significantly affect the plasma insulin response either to glucose or arginine in Groups 1 and 2. Only the glucagon response to arginine was significantly reduced in diabetic hypertensives. Small, non-significant variations in the metabolic and hormonal parameters were seen in additional two groups of patients (Groups 3 and 4), matched with Groups 1 and 2 for age, sex and diseases, who took capsules containing placebo. Thus, nicardipine did not produce any significant overall alteration in glucose homoestasis when given to elderly diabetic or nondiabetic hypertensive subjects.
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PMID:Nicardipine does not cause deterioration of glucose homoeostasis in man: a placebo controlled study in elderly hypertensives with and without diabetes mellitus. 150 7

The paper is devoted to a study of the time course of lipid metabolism, analysis of glucose tolerance, change in indices of immunoreactive insulin, glucagon and C-peptide before the start of verapamil therapy and 6 mos. after it during monotherapy with this drug. These parameters were investigated in the blood serum using biochemical methods and radioimmunoassays. A marked antihypertensive effect was achieved in patients suffering from noninsulin dependent diabetes mellitus with concomitant essential hypertension of the 2nd degree. No negative effect on the pancreatic hormone secretion was noted. Lipid transport indices were improved.
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PMID:[Use of finoptin in patients with non-insulin-dependent diabetes mellitus with concomitant essential hypertension]. 178 2

In 40 patients (pts) with essential hypertension (EH) the plasma levels of insulin, glucagon, gastrin and prolactin during 2 week therapy with nifedipine were evaluated. In pts with EH there were higher levels of hormones than in control subjects. During nifedipine therapy there was no elevation of the plasma hormone levels although the blood pressure was lowered. This study shows that there are other than hypertension factors in the pathogenesis of elevated hormone levels in EH.
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PMID:[Essential hypertension. Treatment with nifedipine and levels of insulin, glucagon, gastrin and prolactin]. 194 46

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

Although it is well known that calcium channel blockers can influence contraction of vascular smooth muscle, there is less knowledge on its effect on excitation contraction coupling in the endocrine glands and more specifically on insulin and glucagon release. In this study, nifedipine was administered in doses of 40 to 80 mg/day to 14 patients with essential hypertension, and its hemodynamic effects were evaluated by non-invasive methods, and its effect on glucose metabolism by an arginine infusion test. Nifedipine produced a significant reduction in systolic and diastolic blood pressure, both after the first dose (30/12 mm Hg) and after 8 weeks of administration (19/12 mm Hg). There were no significant changes in cardiac output (5.1 to 4.9 L/min), muscle (2.4 to 3.2 mL/sec/min) or cutaneous basal flow (9.8 to 8.6 mL/100 mL) as measured non-invasively by echocardiogram and by plethysmography. Insulin and glucagon release were evaluated by the arginine infusion test. Nifedipine produced a tendency toward an increase in glucagon release and a reduction in insulin release although these changes did not reach statistical significance. In this group of patients, nifedipine produced a significant reduction in systolic and diastolic pressure, but no significant changes in insulin or glucagon plasma levels.
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PMID:Hemodynamic and endocrine effects of acute and chronic administration of nifedipine. 265 87

Although it is well known that calcium channel blockers can influence contraction of vascular smooth muscle, there is less knowledge on its effect on excitation contraction coupling in the endocrine glands and more specifically on insulin and glucagon release. In this study, nifedipine was administered in doses of 40 to 80 mg/day to 14 patients with essential hypertension, and its hemodynamic effects were evaluated by non-invasive methods, and its effect on glucose metabolism by an arginine infusion test. Nifedipine produced a significant reduction in systolic and diastolic blood pressure, both after the first dose (30/12 mm Hg) and after 8 weeks of administration (19/12 mm Hg). There were no significant changes in cardiac output (5.1 to 4.9 L/min), muscle (2.4 to 3.2 mL/sec/min) or cutaneous basal flow (9.8 to 8.6 mL/100 mL) as measured non-invasively by echocardiogram and by plethysmography. Insulin and glucagon release were evaluated by the arginine infusion test. Nifedipine produced a tendency towards an increase in glucagon release and a reduction in insulin release although these changes did not reach statistical significance. In this group of patients, nifedipine produced a significant reduction in systolic and diastolic pressure, but no significant changes in insulin or glucagon plasma levels.
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PMID:Hemodynamic and endocrine effects of acute and chronic administration of nifedipine. 265 99

A group of 20 patients with primary hypertension (NT) were studied for the influence of six-week propranolol therapy on the secretion of immunoreactive insulin (IR-I), gastrin glucagon (IR-G) and pancreatic polypeptide (IR-PP) induced by a high-fat test meal. The results of the examination before the therapy were compared with examination of 10 healthy persons. Before the therapy, the patients with NT revealed a decreased reactivity of IR-PP to the food stimulus. After propranolol therapy, the authors found a significant change of glucagonemia profile and pancreatic polypeptide concentration induced by a test meal. The results of the examinations made suggest a direct or indirect participation of beta-adrenergic endings in the regulation of glucagon and pancreatic polypeptide secretion in patients with primary hypertension.
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PMID:[Effect of propranolol therapy on the secretion of insulin, glucagon, gastrin and pancreatic polypeptide in patients with essential hypertension]. 269 15

Studies were performed to explore the effect of calcium antagonism with felodipine for 8 weeks on glucose homeostasis and serum lipids in 8 patients with essential hypertension. Fasting levels of blood glucose as well as serum C-peptide, insulin, glucagon and free fatty acids were unchanged following felodipine. During an intravenous glucose tolerance test, the incremental area under the curve for C-peptide and glucose was unchanged, but decreased for insulin, after felodipine. The decremental area over the curve for glucagon and free fatty acids remained unchanged. Fasting serum total cholesterol and high density lipoprotein cholesterol were unaltered, whereas triglycerides decreased following felodipine. The findings indicate that calcium antagonism with felodipine does not affect glucose-induced insulin release in vivo. The increased insulin clearance could be expected to be coupled to a change in glucose tolerance, but this was unaltered during long-term calcium antagonism.
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PMID:Unchanged insulin secretion and glucose tolerance but increased insulin clearance during long-term calcium antagonism with felodipine in essential hypertension. 331 61


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