Hyperinsulinemia in rats with hypothalamic obesity: effects of autonomic drugs and glucose

1983 ◽  
Vol 245 (3) ◽  
pp. R372-R378 ◽  
Author(s):  
S. Inoue ◽  
Y. S. Mullen ◽  
G. A. Bray
Keyword(s):  
Adrenergic Receptors ◽  
Serum Insulin ◽  
The Other ◽  
Glucose Stimulation ◽  
Hypothalamic Obesity ◽  
Insulin Levels ◽  
Alpha Adrenergic Receptors ◽  
Beta Receptors ◽  
Increased Sensitivity ◽  
Stimulation Of

The present study examined the effects of autonomic drugs and glucose on the insulin and glucose concentrations of sham-operated rats and of rats with ventromedial hypothalamic (VMH) lesions and obesity. In the basal condition both epinephrine and atropine significantly decreased serum insulin levels in VMH-lesioned but not sham-operated rats. During glucose stimulation of insulin secretion in VMH-lesioned rats, epinephrine inhibited the increase of insulin by 83% and atropine inhibited it by 42%; whereas in sham-operated rats, epinephrine inhibited it by 70% and atropine inhibited it by 34%. Epinephrine with atropine completely blocked the increase of insulin in response to glucose in both VMH-lesioned and sham-operated rats. In the basal condition, epinephrine together with propranolol significantly decreased serum insulin levels in VMH-lesioned but not sham-operated rats. Epinephrine with phentolamine, on the other hand, markedly increased insulin in the VMH-lesioned rats and to a lesser degree in the sham-operated rats. During glucose stimulation epinephrine with propranolol inhibited the increase of insulin in both groups. Epinephrine with phentolamine or isoproterenol markedly increased serum insulin in VMH-lesioned rats. These results suggest that stimulation of the vagus nerve and increased sensitivity of the beta-receptors on the beta-cells of the islet contribute to the development of hyperinsulinemia. The sympathetic contribution may also be through suppression of alpha-adrenergic receptors.

Cardiac effects of injections of epinephrine into the spinal intermediolateral column

1993 ◽  
Vol 265 (2) ◽  
pp. H633-H641 ◽  
Author(s):  
V. K. Malhotra ◽  
A. Kachroo ◽  
H. N. Sapru
Keyword(s):  
Adrenergic Receptors ◽  
Cardiovascular Responses ◽  
Spinal Level ◽  
Cardiac Effects ◽  
Alpha Adrenergic Receptors ◽  
Small Doses ◽  
The Right ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Stimulation Of

Small doses of epinephrine (0.008, 0.05, and 0.1 pmol, i.e., 20-nl volumes of 0.40, 2.5, and 5 microM solutions) produced a dose-dependent increase in heart rate when micro-injected into the right intermediolateral column (IML) at T2 spinal level. These effects were mediated via alpha 1-adrenergic receptors because prazosin blocked them. The presence of alpha 1-adrenergic receptors at this site was confirmed by microinjections of phenylephrine (a specific agonist for these receptors); phenylephrine elicited tachycardia. Larger doses of epinephrine (320, 2,000, and 3,200 pmol, i.e., 20-nl volumes of 16, 100, and 160 mM solutions) caused bradycardia when microinjected into the IML. These effects were mediated via alpha 2-adrenergic receptors because idazoxan blocked them. The presence of alpha 2-adrenergic receptors at this site was confirmed by microinjections of clonidine (a specific agonist for these receptors); clonidine elicited bradycardia. Injections of the vehicle (20 nl of normal saline containing 0.3% ascorbic acid, pH 7.4) did not evoke a response. Epinephrine, prazosin, or idazoxan did not alter the responses to L-glutamate. None of the doses of epinephrine elicited any response when injected intravenously. The aforementioned results provide pharmacological evidence for the presence of alpha 1- and alpha 2-adrenergic receptors in the IML at T2. Thus a basis is provided for investigating the role, if any, of alpha-adrenergic receptors in the IML in mediating cardiovascular responses elicited by the stimulation of different brain stem areas.

scholarly journals Atypical Gastric Ulcer in an Elderly Cocaine User

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Vinaya Gaduputi ◽  
Hassan Tariq ◽  
Ariyo Ihimoyan
Keyword(s):  
Gastric Ulcer ◽  
Adrenergic Receptors ◽  
Mesenteric Arteries ◽  
Cocaine User ◽  
Gastrointestinal Manifestations ◽  
Cocaine Use ◽  
Alpha Adrenergic Receptors ◽  
Gastrointestinal Ischemia ◽  
Stimulation Of

Cocaine or Benzoylmethylecgonine is an alkaloid extracted from the leaves of the Erythroxylon plant, which can cause gastrointestinal ischemia from severe arterial vasoconstriction via stimulation of alpha-adrenergic receptors in the gastric and mesenteric arteries. We report this case of a 65-year-old man who presented with a single massive ulcer at the incisura of the stomach as a result of cocaine use. The size and location of this ulcer were atypical and illustrate the potential for serious gastrointestinal manifestations from cocaine use.

Increased glucose sensitivity of both triggering and amplifying pathways of insulin secretion in rat islets cultured for 1 wk in high glucose

2004 ◽  
Vol 287 (2) ◽  
pp. E207-E217 ◽  
Author(s):  
M. Z. Khaldi ◽  
Y. Guiot ◽  
P. Gilon ◽  
J. C. Henquin ◽  
J. C. Jonas
Keyword(s):  
Insulin Secretion ◽  
High Glucose ◽  
Uncoupling Protein ◽  
Glucose Stimulation ◽  
Rat Islets ◽  
Chronic Hyperglycemia ◽  
Intracellular Ca ◽  
Increased Sensitivity ◽  
Glucose Sensitivity ◽  
Stimulation Of

Chronic hyperglycemia has been shown to induce either a lack of response or an increased sensitivity to glucose in pancreatic β-cells. We reinvestigated this controversial issue in a single experimental model by culturing rat islets for 1 wk in 10 or 30 mmol/l glucose (G10, Controls; or G30, High-glucose islets) before testing the effect of stepwise glucose stimulation from G0.5 to G20 on key β-cell stimulus-secretion coupling events. Compared with Controls, the glucose sensitivity of High-glucose islets was markedly increased, leading to maximal stimulation of oxidative metabolism and both triggering and amplifying pathways of insulin secretion in G6 rather than G20, hence to loss of glucose effect above G6. This enhanced glucose sensitivity occurred despite an approximately twofold increase in islet uncoupling protein 2 mRNA expression. Besides this increased glucose sensitivity, the maximal glucose stimulation of insulin secretion in High-glucose islets was reduced by ∼50%, proportionally to the reduction of insulin content. In High-glucose islets, changes in 45Ca2+ influx induced by glucose and diazoxide were qualitatively similar but quantitatively smaller than in Control islets and, paradoxically, did not lead to detectable changes in the intracellular Ca2+ concentration measured by microspectrofluorimetry (fura PE 3). In conclusion, after 1 wk of culture in G30, the loss of glucose stimulation of insulin secretion in the physiological range of glucose concentrations (G5–G10) results from the combination of an increased sensitivity to glucose of both triggering and amplifying pathways of insulin secretion and an ∼50% reduction in the maximal glucose stimulation of insulin secretion.

Venous and arterial responses to stimulation of beta adrenergic receptors

1965 ◽  
Vol 209 (2) ◽  
pp. 383-389 ◽  
Author(s):  
Francois M. Abboud ◽  
John W. Eckstein ◽  
Ben G. Zimmerman
Keyword(s):  
Blood Flow ◽  
Adrenergic Receptors ◽  
Total Blood ◽  
Small Vessels ◽  
Beta Receptors ◽  
Blood Pressures ◽  
Arterial Responses ◽  
Total Blood Flow ◽  
Arteries And Veins ◽  
Stimulation Of

The effects of intra-arterial injections of isoproterenol on small vessels, arteries, and veins were studied in the paw and muscle of the foreleg of dog. Total blood flow to the foreleg was held constant. Blood pressures were measured in large and small arteries and veins. In some experiments venous outflow from paw and muscle was measured. The small vessel segment was the site of major dilatation. Venodilator responses were small, but they were enhanced when isoproterenol was injected in the presence of venous constriction induced by intra-arterial infusions of norepinephrine. Dichloroisoproterenol and nethalide blocked the dilator responses to isoproterenol in all segments but they did not block the dilator responses to acetylcholine or glyceryl trinitrate. Isoproterenol did not change the distribution of blood flow within the foreleg; responses in muscle and paw were not significantly different. The results indicate that stimulation of beta receptors with isoproterenol causes much more dilatation in small vessels than in veins in the foreleg and that small vessels of both paw and muscle dilate equally.

The responses of rat and guinea pig vas deferens to cocaine

1969 ◽  
Vol 47 (5) ◽  
pp. 469-476 ◽  
Author(s):  
M. M. Vohra
Keyword(s):  
Guinea Pig ◽  
Adrenergic Receptors ◽  
Vas Deferens ◽  
Rat Vas Deferens ◽  
Motor Responses ◽  
Transmural Stimulation ◽  
Alpha Adrenergic Receptors ◽  
Sympathomimetic Amine ◽  
Repeated Doses ◽  
Stimulation Of

Cocaine caused contractions and potentiation of motor responses to transmural stimulation of vas deferens of the rat but not of the guinea pig. Tachyphylaxis was not observed after repeated doses of cocaine to vasa deferentia from both normal and reserpine-treated rats. Pretreatment with reserpine reduced significantly (p < 0.05) the responses to cocaine but abolished completely the responses to tyramine. No catecholamines could be detected spectrophotofluorometrically in reserpine-treated preparations. Contractions following the application of cocaine to vasa deferentia from both normal and reserpine-treated rats were completely abolished by phenoxybenzamine, phentolamine, and tolazoline. Cocaine failed to protect alpha-adrenergic receptors against phenoxybenzamine blockade in reserpine-treated preparations; however, cocaine could still evoke contractions of reserpine-treated preparations protected with noradrenaline against phenoxybenzamine blockade. The evidence presented indicates that cocaine acts as a mixed sympathomimetic on the rat vas deferens preparation. The possibility that cocaine is an indirect-acting sympathomimetic amine could not be ruled out in the present study.

Sympathetic control of Na, K transport in perfused submaxillary main duct of rat

1976 ◽  
Vol 230 (2) ◽  
pp. 341-345 ◽  
Author(s):  
LH Schneyer
Keyword(s):  
Sympathetic Nerve ◽  
Adrenergic Receptors ◽  
Sympathetic Innervation ◽  
Submaxillary Gland ◽  
Sympathetic Control ◽  
Alpha Adrenergic Receptors ◽  
Supramaximal Stimulation ◽  
Net Flux ◽  
K Transport ◽  
Stimulation Of

The effect of stimulating the sympathetic innervation to rat submaxillary gland on ductal transport of Na, K, and water and on transepithelial PD was tested in the main excretory duct during perfusion through its lumen. Stimulation of the sympathetic nerve, supramaximally, caused a decrease of 30-40% in net flux of Na from, and of K to, the lumen in ducts perfused with medium containing Na and K in isotonic concentrations. Net flux of water was unaffected. Transductal PD decreased by about 30% during supramaximal stimulation. Changes in PD and net cation fluxes were reversible. These effects of supramaximal stimulation of the sympathetics on ductal transport resemble those reported to occur after large doses of isoproterenol and suggest an adrenergic secretomotor innervation to the ducts. However, changes in PD evoked by supramaximal stimulation of the sympathetic nerve could not be suppressed with propranolol, but were with phenoxybenzamine, indicating that alpha-adrenergic receptors are primarily involved in mediating at least the electrical responses of duct cells to sympathetic nerve stimulation.

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