title: Oral taurine supplementation prevents the development of ethanol-induced hypertension in rats.
abstract: Taurine is known to lower blood pressure in essential hypertension and some experimental hypertensive models. Taurine has also been reported to activate aldehyde dehydrogenase and to inhibit the elevation of plasma acetaldehyde concentration after ethanol intake. Because acetaldehyde, the first metabolite of ethanol, is suspected to be responsible for many adverse effects of alcohol consumption, we examined the effect of taurine supplementation on ethanol-induced hypertension and abnormalities in the intracellular cation metabolism in Witar-Kyoto rats. In Study 1, systolic blood pressure and intraplatelet free calcium were significantly higher in rats who received 15% ethanol in drinking water than in control rats. Oral taurine supplementation (1% taurine and 15% ethanol in drinking water) completely prevented the development of ethanol-induced hypertension. Intraerythrocyte sodium and intraplatelet free calcium were significantly decreased in taurine-supplemented rats as compared with rats who received 15% ethanol only. In Study 2, hemoglobin-associated acetaldehyde (HbAA) was measured as a marker of protein-bound acetaldehyde. HbAA was significantly elevated in rats who received 5% ethanol in drinking water as compared with control rats. Taurine supplementation (1% taurine and 5% ethanol in drinking water) significantly decreased HbAA. Our findings suggest that the oral supplementation of taurine prevents ethanol-induced hypertension by decreasing protein bound acetaldehyde and altering the cation handling by the membrane.
authors.affiliation: First Department of Internal Medicine, Kobe University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Harada
authors.forename: K
authors.initials: K
authors.lastname: Kitazaki
authors.forename: T
authors.initials: T
authors.lastname: Tsujino
authors.forename: Y
authors.initials: Y
authors.lastname: Watari
authors.forename: S
authors.initials: S
authors.lastname: Iwata
authors.forename: H
authors.initials: H
authors.lastname: Nonaka
authors.forename: T
authors.initials: T
authors.lastname: Hayashi
authors.forename: T
authors.initials: T
authors.lastname: Takeshita
authors.forename: K
authors.initials: K
authors.lastname: Morimoto
authors.forename: M
authors.initials: M
authors.lastname: Yokoyama
mesh_terms: D000079:Acetaldehyde / Q000378:metabolism; D000284:Administration, Oral; D000818:Animals; D001792:Blood Platelets / Q000737:chemistry; D001794:Blood Pressure; D001835:Body Weight; D002118:Calcium / Q000032:analysis; D002492:Central Nervous System Depressants / Q000009:adverse effects* / Q000493:pharmacokinetics; D000431:Ethanol / Q000009:adverse effects* / Q000493:pharmacokinetics; D006454:Hemoglobins / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced / Q000188:drug therapy* / Q000517:prevention & control*; D008297:Male; D051381:Rats; D011921:Rats, Inbred WKY; D012964:Sodium / Q000097:blood / Q000652:urine; D013654:Taurine / Q000494:pharmacology*
chemical_list: D002492:Central Nervous System Depressants; D006454:Hemoglobins; D013654:Taurine; D000431:Ethanol; D012964:Sodium; D000079:Acetaldehyde; D002118:Calcium