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  • 1
    Electronic Resource
    Electronic Resource
    An inhibitory effect of tolbutamide and glibenclamide (glyburide) on the pancreatic islets of normal animals (1974)
    Springer
    Diabetologia 10 (1974), S. 27-35 
    Details
    ISSN: 1432-0428
    Keywords: Insulin secretion ; perifusion ; isolated islets ; sulfonylureas ; intravenous glucose tolerance ; intravenous tolbutamide response ; glucose utilization ; tolbutamide ; glibenclamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tolbutamide and glibenclamide (glyburide) were administered to normal hamsters, mice or rats in daily doses proportional to their body weight and equivalent to those used in human therapy. The animals were sacrificed after 6 to 8 weeks of treatment. Pieces of pancreas or isolated pancreatic islets were incubated or perifused in a medium containing glucose or tolbutamide, with or without Ieucine-114C or glucose-U-14C. The results indicate that the B cells of sulfonylurea treated animals synthesized and released less insulin and oxidized less glucose than those of insulin or saline treated controls. Accordingly, at least in the glibenclamide treated animals, the tolerance for glucose and the insulinogenic response to a glucose load in vivo were suppressed. Although insular function tended to return, to normal after treatment was discontinued, the results reported in this paper do not support the generally accepted view that the lasting therapeutic effectiveness of the sulfonylureas is due to a beta-cytotrophic action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421411
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The serum glucose response to glucagon suppression with somatostatin, insulin or antiglucagon serum in depancreatized rats (1978)
    Springer
    Diabetologia 14 (1978), S. 53-58 
    Details
    ISSN: 1432-0428
    Keywords: Glucagon ; somatostatin ; insulin ; antiglucagon serum ; glucagon suppression ; serum glucose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Total immunoreactive glucagon (IRG) and immunoreactive glucagon of A cell origin (IRGa) were measured in the serum of normal, sham-operated and depancreatized rats, after the administration of three glucagon antagonists: insulin (5–200 mU/rat/h), somatostatin (SRIF; 100 μg/kg/h) and antiglucagon serum (AGS, enough to bind three times the calculated total amount of circulating IRG). Since no differences were noted between the responses of normal and sham-operated animals, the values were pooled and used as controls. Pancreatectomy caused a significant increase in serum glucose, IRGa and total IRG and a significant decrease in serum insulin. AGS and SRIF significantly decreased serum glucose in control, but not in depancreatized rats, even though SRIF caused a significant decrease of IRGa in all animals. SRIF significantly decreased plasma insulin in control rats, but did not modify total IRG secretion in either group. In control rats the minimum effective hypoglycaemic dose of insulin (5 mU/rat/h) may have decreased serum IRGa, but not total IRG. At higher doses (20 mU/rat/h) insulin stimulated glucagon secretion. In depancreatized animals, higher doses of insulin (200 mU/rat/h) were needed to lower serum glucose. On the other hand, a dose of 100 μU/rat/h was sufficient to lower the serum IRG. We conclude that although hyperglucagonaemia may contribute to the hyperglycaemia of the untreated depancreatized rats, the excessive secretion of glucagon is secondary to insulin insufficiency and that, at least in this animal model, the hypoglycaemic action of insulin is only minimally dependent upon its ability to suppress glucagon secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00429708
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Mechanisms mediating insulin-induced hypotension in rats (1996)
    Springer
    Acta diabetologica 33 (1996), S. 263-268 
    Details
    ISSN: 1432-5233
    Keywords: Insulin-induced hypotension ; Adrenergic antagonists ; Ganglionic blockers ; Cholinergic antagonist ; Atropine ; Hexamethonium ; Prazosin ; Atenolol ; L-NAME ; Nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms associated with insulin-induced cardiovascular inhibitory responses were evaluated in untreated normal rats and in normal rats pretreated with an antagonist of nitric oxide (NO) production (L-NAME), with cholinergic, alpha- and beta-adrenergic antagonists, or after ganglionic blockade. Male Wistar rats were anesthetized with a mixture of urethane and alpha-chloralose and placed on a electric heating pad. The femoral artery and vein were cannulated for measurements of mean arterial pressure (MAP), heart rate, plasma glucose, blood sampling, and intravenous injections. Intravenous injection of insulin (5.0 U/kg) in untreated rats resulted in a significant and sustained decrease in arterial blood pressure (average 24%) and in a slight decrease in heart rate. These cardiovascular responses were blocked by L-NAME and by the cholinergic antagonist atropine, suggesting an involvement of NO and the cholinergic receptors, or an effect of insulin on the central nervous system parasympathetic center. The ganglionic blocker hexamethonium attenuated the insulin-induced response. On the other hand, the hypotensive effect of insulin persisted after sympathetic blockade with the alpha-1 antagonist prazosin and the beta-1 antagonist atenolol. We conclude that the insulin-induced decrease in blood pressure is due to both increased cholinergic outflow and to NO production and that an enhanced sympathetic activity possibly mediated by a reactive release of norepinephrine or epinephrine modulates this response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571561
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    The effect of a ventral medial hypothalamic lesion on the insulin-induced hypotensive response in normal rats (1994)
    Springer
    Acta diabetologica 31 (1994), S. 91-97 
    Details
    ISSN: 1432-5233
    Keywords: Insulin ; VMH ; Cardiovascular response ; VMH lesion ; Blood pressure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The cardiovascular responses to insulin-induced hypoglycemia were studied in normal and ventral medial hypothalamic (VMH)-lesioned rats. The goal of this study was to investigate the role of the VMH in mediating the insulin-induced decreases in cardiovascular tone. Male Wistar rats were anesthetized with urethane/chloralose. Following the induction of anesthesia, the trachea, femoral artery, and femoral vein were cannulated. The femoral artery was attached to a pressure transducer for cardiovascular monitoring. The cardiovascular activity was recorded using a Modular Instruments Micro 5000 signal processing system. The mean arterial pressure and pulse pressures and heart rate were evaluated. In control studies, a stable plasma glucose and blood pressure were obtained with urethane/chloralose anesthesia for the duration of the experiments. Insulin (2.0 or 5.0 U/kg) significantly decreased the plasma glucose as well as the blood pressure. In VMH-lesioned rats, the lesions were accomplished by radiofrequency, and the cardiovascular response to insulin-induced hypoglycemia was investigated 1 or 6 weeks later. There was no difference in the cardiovascular response to insulin-induced hypoglycemia between the low or high insulin dose after 1 week in VMH-lesioned animals. The low dose after 6 weeks in VMH-lesioned animals did not produce a change in the mean arterial pressure response compared with controls. The pulse pressure was higher than in the sham-lesioned animals, and the plasma glucose response was greater. The high dose after 6 weeks in VMH-lesioned animals in contrast to sham-lesioned animals led to an increased cardiovascular response instead of a decrease. We propose that the decrease in cardiovascular activity in response to insulin-induced hypoglycemia in normal animals can be attributed to a direct or indirect effect on vascular dilation as well as possibly to an inhibition of sympathetic firing. However, it appears that insulin increases the vascular dilation as well as the parasympathetic tone after 1 week in the VMH-lesioned animals, similar to the findings in sham-lesioned animals. However, after 6 weeks, the insulin-induced decreased cardiovascular tone is minimal. Thus, we believe hat the VMH does not have a direct effect in modulating the insulin-induced decrease in cardiovascular tone, but its destruction appears to influence other regulatory centers.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00570542
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Mechanisms mediating insulin-induced hypotension in rats (1996)
    Springer
    Acta diabetologica 33 (1996), S. 263-268 
    Details
    ISSN: 1432-5233
    Keywords: Key words Insulin-induced hypotension ; Adrenergic antagonists ; Ganglionic blockers ; Cholinergic antagonist ; Atropine ; Hexamethonium ; Prazosin ; Atenolol ; L-NAME ; Nitric oxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The mechanisms associated with insulin-induced cardiovascular inhibitory responses were evaluated in untreated normal rats and in normal rats pretreated with an antagonist of nitric oxide (NO) production (L-NAME), with cholinergic, alpha- and beta-adrenergic antagonists, or after ganglionic blockade. Male Wistar rats were anesthetized with a mixture of urethane and alpha-chloralose and placed on a electric heating pad. The femoral artery and vein were cannulated for measurements of mean arterial pressure (MAP), heart rate, plasma glucose, blood sampling, and intravenous injections. Intravenous injection of insulin (5.0 U/kg) in untreated rats resulted in a significant and sustained decrease in arterial blood pressure (average 24%) and in a slight decrease in heart rate. These cardiovascular responses were blocked by L-NAME and by the cholinergic antagonist atropine, suggesting an involvement of NO and the cholinergic receptors, or an effect of insulin on the central nervous system parasympathetic center. The ganglionic blocker hexamethonium attenuated the insulin-induced response. On the other hand, the hypotensive effect of insulin persisted after sympathetic blockade with the alpha-1 antagonist prazosin and the beta-1 antagonist atenolol. We conclude that the insulin-induced decrease in blood pressure is due to both increased cholinergic outflow and to NO production and that an enhanced sympathetic activity possibly mediated by a reactive release of norepinephrine or epinephrine modulates this response.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571561
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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