MANIPULATIONS OF THE RENIN-ANGIOTENSIN SYSTEM AND INTAKE OF A SWEETENED ALCOHOLIC BEVERAGE AMONG RATS

被引:18
作者
HUBBELL, CL
CHRISBACHER, GA
BILSKY, EJ
REID, LD
机构
[1] Department of Psychology, Rensselaer Polytechnic Institute, Troy
关键词
ANGIOTENSIN-II; ETHANOL; ETHANOL INTAKE; LISINOPRIL; ANGIOTENSIN CONVERTING ENZYME INHIBITORS; ALCOHOL ABUSE; ALCOHOLISM; RATS;
D O I
10.1016/0741-8329(92)90010-8
中图分类号
R194 [卫生标准、卫生检查、医药管理];
学科分类号
摘要
Standard laboratory rats were maintained on a daily regimen involving deprivation of fluids for 22 h followed by a 2-h opportunity to drink water and a sweetened alcoholic beverage. Angiotensin II, in doses ranging from 0.1 to 1.25 mg/kg, dose relatedly decreased rats' mean intake of ethanol. All doses increased rats' mean intake of water. Angiotensin II, 0.25 mg/kg, reliably reduced intake of ethanol when it was presented alone during the 1st h of the daily 2-h drinking session, and reliably increased intake of water when it was subsequently presented alone during the 2nd h. Thus the reduction in intake of ethanol seen when the alcoholic beverage is presented concurrently with water is probably not merely due to the increase in intake of water. Lisinopril, an angiotensin converting enzyme inhibitor, in doses of 0.3, 1.0, and 3.0 mg/kg, dose relatedly decreased intake of ethanol, but only after several days of injections. Concurrent intake of water was increased dose relatedly. When injections of lisinopril ceased, intakes of both ethanol and water took several days to return to control levels. Pretreatment with lisinopril, 3.0 mg/kg, for 8 days, had no effect on subsequent intakes of either water or ethanol. Lisinopril, 3.0 mg/kg, had no effect on rats' intake of a sweet solution without ethanol. These results confirm previous work and extend the data base supporting the idea that the renin-angiotensin system plays a role in modulating intake of ethanol.
引用
收藏
页码:53 / 61
页数:9
相关论文
共 34 条
[21]  
LEENEN FHH, 1984, HDB HYPERTENSION EXP, V4, P24
[22]  
LIND RW, 1985, NEUROENDOCRINOLOGY, V40, P2
[23]   ANGIOTENSIN CONVERTING ENZYME-INHIBITORS REDUCE ALCOHOL-CONSUMPTION - SOME POSSIBLE MECHANISMS AND IMPORTANT CONDITIONS FOR ITS THERAPEUTIC USE [J].
LINGHAM, T ;
PERLANSKI, E ;
GRUPP, LA .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 1990, 14 (01) :92-99
[24]  
MYERS W D, 1984, Alcohol, V1, P229, DOI 10.1016/0741-8329(84)90103-4
[25]   ANGIOTENSIN-II INFUSION INCREASES VASOPRESSIN, ACTH, AND 11-HYDROXYCORTICOSTEROID SECRETION [J].
RAMSAY, DJ ;
KEIL, LC ;
SHARPE, MC ;
SHINSAKO, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1978, 234 (01) :R66-R71
[26]   PLASMA MINERALOCORTICOIDS, PLASMA-RENIN, AND URINARY KALLIKREIN IN SALT-SENSITIVE AND SALT-RESISTANT RATS [J].
RAPP, JP ;
TAN, SY ;
MARGOLIUS, HS .
ENDOCRINE RESEARCH COMMUNICATIONS, 1978, 5 (01) :35-41
[27]   VASOPRESSIN DOES NOT MEDIATE THE INHIBITION OF ETHANOL DRINKING BY THE RENIN-ANGIOTENSIN SYSTEM [J].
ROSS, AD ;
PERLANSKI, E ;
GRUPP, LA .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1990, 36 (04) :761-765
[28]   SODIUM APPETITE - SPECIES AND STRAIN DIFFERENCES AND ROLE OF RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM [J].
ROWLAND, NE ;
FREGLY, MJ .
APPETITE, 1988, 11 (03) :143-178
[29]   MECHANISM OF CAPTOPRIL-INDUCED DRINKING [J].
SCHIFFRIN, EL ;
GENEST, J .
AMERICAN JOURNAL OF PHYSIOLOGY, 1982, 242 (01) :R136-R140
[30]   HYPER-ALDOSTERONISM IN THE SODIUM-DEPLETED RAT - MODE OF ALDOSTERONE-STIMULATING ACTION OF FRUSEMIDE [J].
SPAT, A ;
TARJAN, E ;
TOTH, G .
JOURNAL OF ENDOCRINOLOGY, 1979, 82 (01) :7-15