Chronic sucrose ingestion induces mild hypertension and tachycardia in rats.
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.
D000818:Animals; D005951:Glucose Tolerance Test; D006439:Hemodynamics / Q000187:drug effects; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology; D007328:Insulin / Q000097:blood / Q000378:metabolism; D000078790:Insulin Secretion; D008297:Male; D010179:Pancreas / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013395:Sucrose / Q000633:toxicity*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D013610:Tachycardia / Q000139:chemically induced*
D007328:Insulin; D013395:Sucrose