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Hypertension, Vol 5, 218-225, Copyright © 1983 by American Heart Association
RD Bunag, T Tomita and S Sasaki
As a means for increasing sympathetic activity, male weanling rats were
given 8% sucrose solution to drink instead of water. After 5 weeks,
systolic pressures measured with a tail-cuff method became appreciably
elevated, and the elevation was verified when phasic pressures were later
recorded directly from femoral catheters. Successful induction of
sympathetic overactivity was considered a likely explanation because
sucrose-ingesting rats, compared with untreated controls, had faster heart
rates and larger hypotensive responses to alpha-adrenergic blockade with
phentolamine. Upon graded electrical stimulation of the ventromedial
hypothalamus under urethane anesthesia, resulting pressor and sympathetic
nerve responses were also larger in sucrose-treated rats. By contrast,
pressor responses to injections of norepinephrine or tyramine were
unaffected, thereby indicating that cardiovascular sensitivity had not been
enhanced by sucrose ingestion. During intravenous glucose tolerance tests,
increases in plasma insulin were consistently lower in sucrose-treated than
control rats even though corresponding increases in plasma glucose were
just transiently higher. These results support the interpretation that
chronic sucrose ingestion inhibits pancreatic insulin secretion and
elevates blood pressure by stimulating the ventromedial hypothalamus to
increase sympathetic activity.
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Chronic sucrose ingestion induces mild hypertension and tachycardia in rats
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