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  • 1995-1999  (3)
  • Cholinergic antagonist  (2)
  • Blood pressure  (1)
  • 1
    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
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 2
    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
  • 3
    Electronic Resource
    Electronic Resource
    Effects of general and selective β-adrenergic antagonists on insulin-induced cardiac and selected vascular responses in rats (1999)
    Springer
    Acta diabetologica 36 (1999), S. 53-60 
    Details
    ISSN: 1432-5233
    Keywords: Key words Insulin ; β-adrenergic ; Blood pressure ; Blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Insulin administration results in vasodilation, decreased mean arterial blood pressure (MAP) and increased conductances (flow/MAP) in various vascular beds. β-adrenergic blockers antagonize this response, but the mechanism of the interplay between insulin-induced vasodilation and β-adrenergic antagonism is unknown. In this study, we evaluated the effects of β-blockade using the selective β2 antagonist ICI 118551 or the general β-antagonist propranolol on insulin-induced cardiac and regional flow responses in normal rats. Insulin-induced responses were also examined following adrenalectomy. Rats were anaesthetized and the femoral vein and artery were cannulated for infusions, sampling or monitoring of MAP and heart rate (HR). The iliac, renal, and superior mesentery arteries were equipped with pulsed-Doppler flow probes. Blood samples were collected at selected intervals. Insulin decreased blood glucose, MAP and increased conductances. Pretreatment with propranolol not only antagonized the insulin-induced decrease in MAP and increased conductance but insulin also then increased MAP and decreased conductances. ICI 11851, like propranolol, antagonized the insulin-induced decrease in MAP and increased iliac and renal artery conductances. Adrenalectomy did not alter the maximum insulin-induced effects on MAP and conductances but prevented the rebound recovery phase. β-blockade following adrenalectomy had the same effects as β-blockade alone on the insulin-induced responses. We conclude that the insulin-induced decrease in MAP and the increased flow in the selective vascular beds are modulated by a sympathetic β2-receptor-mediated pathway and this response is not due primarily to the release of adrenal catecholamine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s005920050145
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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