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)

The effects of glucagon in concentrations of 0.294 times 10(-6) mol/l, 1.47 times 10(-6) mol/l; 2.94 times 10(-6) mol/l, 5.8 times 10(-6) mol/l, and 1.47 times 10(-5) mol/l on the simultaneously recorded action potentials and contractions; and microsomal and sarcolemmal Na+-tk+-atpase in the myocardium of the guinea pig, rabbit, dog, and pig were investigated. Glucagon in all the concentrations produced an inhibition of the Na+-K+-ATPase associated with an increase in the contractility and shortening of the duration of action potential in dog myocardium. The increase in contraction was concentration-dependent up to a certain concentration. Inhibition of sarcolemmal ATPase was more than that of microsomal ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase. In none of the concentrations did glucagon produce any significant changes in the Na+-K+-ATPase, contractility, and action potential duration in the myocardium of guinea pig, rabbit, or pig. These results suggest that glucagon-induced positive inotropic effect might be due to an increase in the Ca++ influx as a result of inhibition of membrane Na+-K+-ATPase. Shortening of the action potential duration might also be due to an increased efflux of potassium as a result of an inhibition of Na+-K+-ATPase.
Cardiovasc Res 1975 May
PMID:Glucagon-induced changes in the action potential, contraction, and Na+-K+-ATPase of cardiac muscle. 12 13

Cyclic AMP is a common second messenger for a variety of hormones such as catecholamine, glucagon, and growth hormone, which are affected by cardiac surgery. Changes in plasma cyclic AMP level may thus reflect an altered hormonal milieu. The effects of open-heart surgery on plasma cyclic AMP and its relation with serum insulin were studied in 33 adult patients who underwent cardiac surgery with cardiopulmonary bypass. Plasma cyclic AMP levels were markedly elevated during cardiopulmonary bypass and returned toward normal within several days after the operation. The serum insulin concentration remained low, and no positive correlation was found with plasma cyclic AMP level. The responses were similar in patients who had aorta-coronary bypass grafts and those who had valve replacements.
J Thorac Cardiovasc Surg 1978 Feb
PMID:Levels of plasma cyclic AMP and insulin in cardiac surgery. 20 75

A slow (1.18 mumol.kg-1.mm-1) intravenous infusion of disopyramide (mol.wt 339) was given to 8 adult Beagle dogs. An initial phase of slow decline in cardiac output and broadening of the QRS complex on the ECG, with systolic blood pressure maintained above 13.5 kPa (100 mmHg), was followed by a phase of rapid circulatory failure without a correspondingly dramatic change in ECG appearances. Underventilation and cardiac arrhythmias were observed only in the agonal phase after several minutes of circulatory arrest. They were not therefore the primary cause of death, which was due to failure of myocardial contractility. Three positively inotropic drugs (isoprenaline, dopamine, and glucagon) are shown to be capable of restoring the failing circulation, provided they are given before the phase of complete circulatory standstill. In this respect isoprenaline appears superior to dopamine and glucagon.
Cardiovasc Res 1979 Nov
PMID:Cardiac consequences and treatment of disopyramide intoxication: experimental evaluation in dogs. 51 65

The effects of glucagon on quinidine-induced cardiac toxicity were studied in open-chest anaesthetised dogs. Glucagon along increased the heart rate and contractility; and decreased the blood pressure, duration of P-R and Q-T interval, and QRS complex. Quinidine produced dose-dependent decreases in the heart rate, blood pressure, and contractility, and lengthening of the duration of P-R and Q-T interval, and QRS complex. Glucagon abolished the changes produced by quinidine within two minutes, and appears to be a drug of choice in the treatment of quinidine toxicity in the heart.
Cardiovasc Res 1977 Jan
PMID:Use of glucagon in the treatment of quinidine toxicity in the heart. 83 87

In order to study the haemodynamic effects of isoprenaline and glucagon in the immediate postoperative period, 16 patients who had single or multiple valve replacement or coronary artery bypass grafts were investigated. Measurements of cardiac index, stroke index, heart rate, arterial and right atrial mean pressures were made either before, during, or after the administration of both drugs. With the doses used, the inotropic effects of both drugs are similar, while the chronotropic action is statistically higher during isoprenaline infusion than after glucagon administration. This fact explains the greater increase in cardiac index after isoprenaline administration. Mean arterial pressure shows no significant changes after either drug, while right atrial mean pressure decreases significantly. Peripheral vascular resistance remained mostly constant. The activity of glucagon injected as a single bolus seems to be maximal 10 to 15 minutes after the injection and dissipates about 30 minutes later. The ideal dose of isoprenaline is between 0.8 and 2 mug/min. Within this range, the inotropic effect is maximal and the chronotropic and bathmotropic effects are limited. Above 2 mug/min, cardiac index and stroke index decrease, and arrhythmias become more frequent.
Scand J Thorac Cardiovasc Surg 1975
PMID:Comparative haemodynamic effects of glucagon and isoprenaline in the early postoperative period in cardiac surgery. 120 6

Adult white rabbits were subjected to 2 hours of partial cardiopulmonary bypass (flow rate 90 ml/min/kg) at 32 degrees C, and unilateral pulmonary artery occlusion was used to simulate total cardiopulmonary bypass in the lung subjected to arterial occlusion, with the other side used as the control lung. The lung subjected to arterial occlusion was reperfused by one of the following methods: (1) by whole blood (WB group), (2) by leukocyte-depleted blood (LD group), and (3) by whole blood with protease inhibitor (nafamostat mesilate, FUT group), expecting its anticomplement action. In the fourth group, the lung was inflated with oxygen during pulmonary artery occlusion followed by whole blood reperfusion (OXY group). As a result, lungs subjected to pulmonary artery occlusion showed significant decreases in tissue concentrations of adenosine triphosphate and regional tissue blood flow during cardiopulmonary bypass. Furthermore, recovery of adenosine triphosphate was depressed in the WB group and recovery of regional tissue blood flow in the WB and OXY groups. Ultrastructural findings in alveolar epithelial cells and capillary endothelial cells showed worsening at reperfusion in only the WB group. Transpulmonary gradients of C5a and leukocyte showed significant increases at reperfusion in the WB and OXY groups. Alveolar-arterial oxygen difference was significantly higher in the WB group than in the others. Results indicate that complete cessation of pulmonary artery flow in normothermic cardiopulmonary bypass may cause ischemia of the lung followed by reperfusion injuries with the no-reflow phenomenon, with possible involvement of activation of leukocytes and complement.
J Thorac Cardiovasc Surg 1992 Mar
PMID:Experimental study in a rabbit model of ischemia-reperfusion lung injury during cardiopulmonary bypass. 154 56

The present study investigated whether in vivo endogenous opioids inhibit the secretory activity of pheochromocytomas and whether opioid antagonists may be useful in the diagnosis of pheochromocytoma. In six patients with pheochromocytoma in whom the diagnosis was histologically confirmed after surgery, mean intraarterial blood pressure (BP) increased by 45 mm Hg within 3 min after intravenous (i.v.) injection of 2 mg glucagon (95% confidence interval 23-68 mm Hg); heart rate (HR) remained unchanged, whereas plasma norepinephrine (NE) increased by 216% (31-658%) and plasma epinephrine (EPI) increased by 203% (37-571%). Although glucagon stimulation confirmed the secretory potential of the pheochromocytomas, opioid antagonism by a 10-mg i.v. bolus of naloxone produced no significant change in plasma NE and EPI concentrations or intraarterial pressure. The present study does not support the hypothesis that release of catecholamines from pheochromocytomas is inhibited by endogenous opioids. Use of opioid antagonists as a tool in the diagnosis of pheochromocytoma therefore cannot be recommended.
J Cardiovasc Pharmacol 1990 Mar
PMID:Influence of opioid antagonism on plasma catecholamines in pheochromocytoma patients. 169 61

Previous studies have shown that left ventricular (LV) hypertrophy in renal hypertensive rats (RHR) is associated with reduced responsiveness to beta-adrenergic stimulation (isoproterenol) but not to calcium or cardiac glycosides. To determine whether this impairment is restricted to beta-receptor agonists or extended to include other stimulants of the adenylate cyclase system, inotropic responses to glucagon and to vasoactive intestinal peptide (VIP) were determined in isolated paced hearts (Langendorff preparation) from RHR and strictly matched sham-operated controls. The response (delta peak LV +dP/dt) to both agonists was significantly reduced in RHR, whether expressed in absolute value or in percent of baseline. It averaged 59.3 +/- 19.3 (SE) mm Hg X s-1 in RHR at the highest dose of VIP (15 micrograms) and a perfusion pressure (PP) of 50 mm Hg as compared with 255 +/- 68.4 in controls (p less than 0.01). The responses to glucagon were determined at two levels of perfusion pressure--50 and 80 mm Hg--to determine the influence, if any, of possible alterations in myocardial perfusion on differences between the normal and hypertrophied hearts. At both PP levels the LV +dP/dt response was significantly lower in RHR--+ 374 +/- 103 vs. + 1,026 +/- 166 mm Hg X s-1 (p less than 0.005) or + 120 +/- 5 vs. + 143 +/- 7% of baseline value (p less than 0.02) for PP of 50 mm Hg; and 392 +/- 154 vs. + 1,732 +/- 251 mm Hg X s-1 (p less than 0.01) or + 112 +/- 4 vs. + 160 +/- 2% (p less than 0.001) for PP of 80 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol
PMID:Inotropic responsiveness in hypertensive left ventricular hypertrophy: impaired inotropic response to glucagon and vasoactive intestinal peptide in renal hypertensive rats. 242 81

The adrenergic control of carbohydrate metabolism is expressed at two levels: regulation of substrate flow, and interference with the secretion of hormones. Normally, this adrenergic regulatory system only plays a minor role. However, it is of great importance as an acute adaptation of the body to fight and flight. Under these circumstances, fuel fluxes increase almost instantaneously. Glycogenolysis and gluconeogenesis are responsible for increased hepatic glucose output. Increased fatty acid flux is brought about by stimulated adipose tissue lipolysis, which probably, as a secondary phenomenon, causes decreased peripheral glucose utilisation by the skeletal muscle mass. Cerebral glucose uptake accounts for half the body's basal glucose production. Since this glucose uptake is concentration-dependent only, hypoglycaemia rapidly leads to cerebral dysfunction. To guarantee cerebral glucose uptake, the body has a dual defense mechanism against hypoglycaemia: hormonal and metabolic counteraction. The first consists of the secretion of glucagon and (nor)epinephrine, the latter of hepatic autoregulation and alternative fuels for noncerebral tissues. In clinical practice, the inappropriate insulin-excess state forms the major cause of hypoglycaemia. There is, however, a second reason why patients with diabetes mellitus are at risk. Diabetes by itself leads to impaired glucagon secretion and, when autonomic neuropathy exists, to diminished (nor)epinephrine secretion. Thus, interference with the latter, such as administration of beta-blocking agents, further impairs hypoglycaemic counterregulation. In fact, numerous studies document delayed recovery from experimentally induced hypoglycaemia in diabetic patients receiving beta-blocking agents. However, using beta 1-selective blocking agents, mean recovery from hypoglycaemia in groups of diabetic patients demonstrates minor delay only.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1986
PMID:Beta-blockade and carbohydrate metabolism: theoretical aspects and clinical implications. 243 7

Intracellular Ca2+ influx is an essential step in insulin (I) release. Calcium antagonists are reported to reduce I release in vitro and in patients with impaired glucose tolerance (IGT) during acute administration. Their effects during long-term therapy are still controversial. To evaluate the effects of chronic verapamil (V) and nifedipine (N) on carbohydrate metabolism, 12 hypertensive patients (WHO II; aged 37-64 years) with IGT underwent intravenous glucose tolerance tests (IVGTT) (0.33 g/kg body weight in 3 min), arginine (A) infusion (30 g/30 min), and hypoglycemic stress (regular insulin 0.15 U/kg body weight) during which blood levels of glucose (G), I, growth hormone (GH), glucagon (IRG), and cortisol (C) were measured. The patients were then randomized to V (120 mg b.i.d.) or N (20 mg b.i.d.) treatment and, 1 month later, both IVGTT and A infusion were repeated. Hormone determinations were performed by the radioimmunoassay (RIA) and G by the enzymatic method. The patients were maintained on their usual diet for the duration of the study. The rate of decline of G during IVGTT was expressed as Conard's K coefficient (K; normal values greater than 1.3). I and GH during IVGTT were evaluated as the differences between basal and peak values. I, IRG, and GH during A infusion were analyzed as incremental areas. Our results show that neither V nor N impaired carbohydrate metabolism in hypertensive patients with IGT.
J Cardiovasc Pharmacol 1987
PMID:Effect of nifedipine and verapamil on carbohydrate metabolism in hypertensive patients with impaired glucose tolerance. 245 32


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