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  • 1
    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
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  • 2
    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
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