Drugs online research references
Pharmacol Biochem Behav. 1988 Aug;30(4):823-7.
Attenuation of alcohol intake by a serotonin uptake inhibitor: evidence for mediation through the renin-angiotensin system.
Grupp LA, Perlanski E, Stewart RB.
Department of Pharmacology, University of Toronto, Ontario, Canada.
Although the serotonin uptake inhibitors have been shown to reduce alcohol intake in both animals and man, the mechanism of this effect is unclear. It is known that enhanced serotonergic activity can stimulate activity in the renin-angiotensin system and that elevated activity in the renin-angiotensin system can reduce voluntary alcohol intake. Therefore, serotonin uptake inhibitors such as fluoxetine might exert their effect on alcohol intake, in part, through the renin-angiotensin system. The present experiment assesses this possibility by examining the effect of the angiotensin converting enzyme inhibitor, enalapril, on the fluoxetine-induced decrease in alcohol intake. Four groups of rats were offered limited access to alcohol for 1 hr each day. When intake stabilized each group was injected with 2.5, 5.0 or 10.0 mg/kg of fluoxetine or the saline vehicle 1 hr prior to the access to alcohol. Fluoxetine produced a dose-dependent decrease in alcohol intake. Following this, all groups received injections of 1 mg/kg of the angiotensin converting enzyme inhibitor, enalapril, 40 min prior to the fluoxetine. Enalapril had no effect on alcohol intake in the saline group, but reversed the suppression in alcohol intake produced by the 2.5 mg/kg and 5.0 mg/kg doses of fluoxetine and partially reversed the effect of the 10.0 mg/kg dose. These findings indicate that the fluoxetine-induced reduction in alcohol intake may, in part, be mediated through the renin-angiotensin system.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2852370&dopt=Abstract
Scand J Urol Nephrol Suppl. 1984;79:29-34.
The influence of sodium intake on physiological responses to angiotensin II in conscious dogs.
Olsen ME, Meydrech EF.
The renin-angiotensin system (RAS) is suppressed either by high sodium intake or by high levels of angiotensin II (A II). Therefore in prior studies it has been difficult to sort out the influence on the cardiovascular homeostases of different levels of A II and different levels of sodium in the diet respectively. The present study examines the quantitative effects of A II on mean arterial blood pressure (MABP), electrolyte excretion and hormone secretion in conscious dogs on low, normal and high sodium intake with the endogenous RAS blocked with continuous intravenous infusion of enalapril (MK-421). Fourteen dogs on three different Na diets, low, normal and high (5, 30 and 250 mmol/day), were infused continuously with enalapril, 4 mg/kg/day and studied with superinfused A II at rates of 0, 1, 3, 6 and 12 ng/kg/min., each period lasting one week. Converting enzyme inhibitor (CEI) decreased MABP equally in dogs on low and normal sodium intake to about 80% of control, but did not have a significant effect in dogs on high sodium intake. The initial infusion of angiotensin II at the lowest rate had a pronounced effect on MABP in the normal and high sodium states, but had no effect on MABP in the sodium depleted dogs. However, at the higher rates of infusion, the angiotensin II increased the pressure to a similar degree at all levels of sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)
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Brain Res. 1995 Jan 9;669(1):73-8.
Bradykinin-induced water intake and brain fos-like immunoreactivity in rats.
Rowland NE, Fregly MJ, Cimmerer AL.
Department of Psychology, University of Florida, Gainesville, 32611-2250.
We have previously shown that peripheral injection of bradykinin in combination with the kininase II inhibitor, captopril, to rats produces a robust water intake. We now extend this observation to another kininase II inhibitor, enalapril. Water intake increases with dose of dose of bradykinin, but has an inverted U-shaped relationship with dose of kininase II inhibitor. The induced water intake is completely blocked by peripheral administration of the bradykinin antagonist, Hoe 140, and is partly attenuated by peripheral injection of an angiotensin (Ang) II receptor antagonist, losartan. Relative to captopril alone, the combination of captopril and bradykinin greatly elevated plasma renin activity, but did not reduce blood pressure. We further show that, while either bradykinin or enalapril alone induce little or no Fos-like immunoreactivity in areas of the brain related to fluid balance, their combination induces staining in many cells in the supraoptic and paraventricular magnocellular nuclei, as well as along the lamina terminalis. These data suggest that bradykinin may have a role in regulation of fluid balance, partly mediated through Ang II.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7712167&dopt=Abstract
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