Effect of Acute Administration of Prazosin on Blood Pressure, Heart Rate and Plasma Renin Level in the Conscious Normotensive Rat

Atkinson, Jeffrey; Luthi, P.; Sonnay, Mireille; Boillat, Nicole

doi:10.1111/j.1440-1681.1986.tb00936.x

Cited by 7 publications

(7 citation statements)

References 23 publications

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“…The inhibition of the plasma renin response to graded haemorrhage by central choline was associated with enhanced plasma vasopressin and catecholamine responses to haemorrhage, which agree well with previous observations 5,12 . It has long been known that vasopressin inhibits, 18,25–28 whereas catecholamines stimulate, 18,29–32 renal renin secretion and PRA. The observed significant elevation in PRA in the first two blood samples following pretreatment of control rats with the vasopressin receptor antagonist agrees well with these previous studies 18,25–28 and indicates the presence of tonic inhibition by plasma vasopressin on renin secretion and PRA.…”

Section: Discussionsupporting

confidence: 90%

“…administration of choline increases plasma catecholamine concentrations, 33,34 the observed increase in the plasma renin response to graded haemorrhage following i.p. administration of 90 mg/kg choline may also have resulted from the catecholamine‐induced stimulation of renin release, 18,29–32 as shown with peripheral physostigmine 14 . This view is further supported by the observation that pretreatment with propranolol (1 mg/kg, i.p.…”

Section: Discussionmentioning

confidence: 79%

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Central Choline Suppresses Plasma Renin Response to Graded Haemorrhage in Rats

Isbil-Buyukcoskun

İlçöl²,

Cansev

et al. 2008

Clin Exp Pharma Physio

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Central administration of choline increases blood pressure in normotensive and hypotensive states by increasing plasma concentrations of vasopressin and catecholamines. We hypothesized that choline could also modulate the renin-angiotensin pathway, the third main pressor system in the body. Plasma renin activity (PRA), which serves as an index of the function of the peripheral renin-angiotensin system, was determined in rats subjected to graded haemorrhage following central choline administration. Intracerebroventricular (i.c.v.) injection of choline (12.5-150 microg), a precursor of the neurotransmitter acetylcholine (ACh), inhibited the increase in PRA in rats subjected to graded haemorrhage by sequential removal of 0.55 mL blood/100 g bodyweight. Choline, in the range 50-150 microg, increased blood pressure. Intraperitoneal (i.p.) administration of 150 microg choline failed to alter blood pressure and plasma renin responses to graded haemorrhage. Administration of a higher dose (90 mg/kg, i.p.) of choline decreased blood pressure and enhanced PRA in the first two blood samples obtained during the graded haemorrhage. Physostigmine (10 microg, i.c.v.), ACh (10 microg, i.c.v.), carbamylcholine (10 microg, i.c.v.) and cytidine 5'-diphosphocholine (CDP-choline; 250 microg, i.c.v.) increased blood pressure and attenuated plasma renin responses to graded haemorrhage. Inhibition of PRA by i.c.v. choline was abolished by i.c.v. pretreatment with mecamylamine (50 microg), but not atropine (10 microg). Blood pressure responses to choline (150 microg) were attenuated by pretreatment with both mecamylamine and atropine. Inhibition of PRA in response to central choline administration was associated with enhanced plasma vasopressin and catecholamine responses to graded haemorrhage. Pretreatment of rats with a vasopressin antagonist reversed central choline-induced inhibition of plasma renin responses to graded haemorrhage without altering the blood pressure response. In conclusion, central administration of choline inhibits the plasma renin response to graded haemorrhage. Nicotinic receptor activation and an increase in plasma vasopressin appear to be involved in this effect.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 79%

Central Choline Suppresses Plasma Renin Response to Graded Haemorrhage in Rats

Isbil-Buyukcoskun

İlçöl²,

Cansev

et al. 2008

Clin Exp Pharma Physio

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“…The increase in water intake could be due to prazosin-induced activation of the renin-angiotensin system. Prazosin can induce a small transient rise in plasma renin and angiotensin in both humans and rats, regardless of whether a change in blood pressure occurs (Atkinson et al, 1986; McAreavey et al, 1981), although a rise is not always seen (Koshy et al, 1977; Webb et al 1987). Activation of the renin-angiotensin system results in thirst and leads to increased water intake (for review see Evered, 1983).…”

Section: Discussionmentioning

confidence: 99%

Prazosin Reduces Alcohol Drinking Throughout Prolonged Treatment and Blocks the Initiation of Drinking in Rats Selectively Bred for High Alcohol Intake

Froehlich

Hausauer

Federoff

et al. 2013

Alcohol Clin Exp Res

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BACKGROUND This study examined whether prazosin reduces alcohol drinking over the course of prolonged treatment and whether it blocks initiation of alcohol drinking in rats with a genetic predisposition toward high alcohol drinking, i.e, alcohol-preferring (P) rats. METHODS In study one, alcohol-experienced P rats that had been drinking alcohol 2 hrs/day for several months were treated daily with prazosin (0, 0.5, 1.0 or 2.0 mg/kg BW) for 7 weeks. In study two, alcohol-naïve P rats were treated daily with prazosin (0, 1.0 or 2.0 mg/kg BW) for two weeks prior to, or concomitantly with, initiation of alcohol access and throughout 3 weeks of alcohol availability. Prazosin treatment and alcohol access were then discontinued for 2 weeks followed by reinstatement of alcohol access without prazosin treatment for 4 weeks, followed by resumption of daily prazosin treatment (2.0 mg/kg BW) for 3 weeks. RESULTS Prazosin reduced alcohol drinking throughout 7 weeks of treatment in P rats accustomed to drinking alcohol. Following termination of prazosin treatment, alcohol drinking slowly returned to pretreatment baseline. Reduced alcohol intake was accompanied by increased water intake. In alcohol-naïve P rats, prazosin administration prior to the first opportunity to drink alcohol and throughout 3 weeks of alcohol access retarded acquisition of alcohol drinking and reduced the amount of alcohol consumed. When prazosin was administered concomitantly with the first opportunity to drink alcohol, it abolished acquisition of alcohol drinking. Discontinuation of prazosin treatment allowed expression of a genetic predisposition toward high alcohol drinking to gradually emerge. Prazosin retained the ability to reduce alcohol intake with repeated treatments. CONCLUSIONS Prazosin decreased alcohol drinking during prolonged treatment and may be useful for treating alcoholism and alcohol use disorders. Prazosin may also be useful for deterring initiation of drinking in individuals with a family history of alcoholism.

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“…Apparently this was not the case for prazosin at doses which efficiently lower blood pressure in the rat [1], Sleepiness is also no major side effect in patients treated with prazosin [for review see 4], The same holds for guanfacine, a centrally a 2-adrenergic stimulating antihypertensive drug [9], The prolongation of waking with active EMG by prazosin arguments against the assumption that the ai-affinity of tricyclic psychotropic drugs is the reason for the sedative effect of these drugs. Presumably anticholinergic, antihistaminic, dopaminolytic or some other effects are more important with regard to 'sedation'.…”

Section: Discussionmentioning

confidence: 99%

Effects of the Selective α<sub>1</sub>-Adrenoceptor Blocker Prazosin on EEG Sleep and Waking Stages in the Rat

Kleinlogel¹

1989

Neuropsychobiology

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In order to gain a better understanding of the role of the noradrenergic system in the control of the EEG sleep-waking stages, the effects of the selective α₁-antagonist prazosin was investigated in the rat. Oral doses of prazosin (0.1–10 mg/kg) were administered that have been shown to enter the brain. EEG sleep and waking stages were recorded either during 8 h after drug administration at 8.00 in the morning or during 48 h after drug administration at 16.00 in the afternoon. It was found that prazosin at doses of 0.1–10 mg/kg shortened quiet waking. Starting at 1 mg/kg paradoxical sleep (PS) was shortened and, most interestingly, active waking and slow wave sleep (SWS) were prolonged. PS spindles and dozing were shortened after a latency of some hours during the 48-hour experiment. However, during the 8-hour experiment PS spindles were prolonged at 0.32 and 1 mg/kg. These data suggest that in the rat α₁-adrenoceptor inhibition in the brain allows the occurrence of active waking and SWS and suppresses PS.

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Effect of Acute Administration of Prazosin on Blood Pressure, Heart Rate and Plasma Renin Level in the Conscious Normotensive Rat

Cited by 7 publications

References 23 publications

Central Choline Suppresses Plasma Renin Response to Graded Haemorrhage in Rats

Central Choline Suppresses Plasma Renin Response to Graded Haemorrhage in Rats

Prazosin Reduces Alcohol Drinking Throughout Prolonged Treatment and Blocks the Initiation of Drinking in Rats Selectively Bred for High Alcohol Intake

Effects of the Selective α<sub>1</sub>-Adrenoceptor Blocker Prazosin on EEG Sleep and Waking Stages in the Rat

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