Document Detail

Dopaminergic modulation of the pressure-natriuresis response in rats.
MedLine Citation:
PMID:  1325507     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: The present study was carried out to examine the involvement of dopamine in the pressure-natriuresis phenomenon which has been postulated as a major regulator of extracellular fluid volume and thereby arterial pressure. DESIGN: Dopaminergic modulation of the pressure-natriuresis response was studied in the innervated and denervated rat kidney, to allow a distinction between the effects of neural and extraneural dopamine. METHODS: The pressure-natriuresis response was studied in anesthetized Sprague-Dawley rats, in which neural and hormonal influences on the kidney were fixed by denervating the kidney and by intravenous infusion of aldosterone, hydrocortisone, vasopressin and norepinephrine. The innervation to the kidney remained intact in some experiments with the selective dopamine-1 antagonist SCH 23390. Urinary excretion of dopamine during the pressure-natriuresis response was also examined in the innervated and denervated rat kidney. RESULTS: Although infusion of dopamine at a dose of 2 micrograms/kg per min had no effect on the pressure-natriuresis response in rats in which neural and hormonal influences on the kidney were fixed, the slopes of the relations between urine flow, sodium excretion and mean arterial pressure in rats given 10 micrograms/kg per min dopamine were significantly greater than those found in the control rats. Renal plasma flow increased significantly in the dopamine-treated rats whilst glomerular filtration rate did not differ between the control and dopamine-treated rats. The dopamine-induced increase in the slope of pressure-natriuresis relationship and renal plasma flow were completely blocked by 0.5 micrograms/kg per min SCH 23390. However, infusion of SCH 23390 alone at 0.5 micrograms/kg per min did not significantly alter the pressure-natriuresis response in rats with either denervated or innervated kidney. In addition, urinary excretion of dopamine derived from neither neural nor extraneural origins was altered in parallel with variations in mean arterial pressure. CONCLUSION: These results suggest that exogenous administration of dopamine may affect the pressure-natriuresis response by altering the magnitude of arterial pressure-induced changes in tubular sodium reabsorption, via an action of dopamine-1 receptors. However, endogenous dopamine does not appear to be capable of modulating the pressure-natriuresis response.
S Yuasa; H Bandai; T Yura; T Sumikura; N Takahashi; K Uchida; S Miki; Y Takamitsu; H Matsuo
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of hypertension     Volume:  10     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  1992 Aug 
Date Detail:
Created Date:  1992-10-08     Completed Date:  1992-10-08     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  757-63     Citation Subset:  IM    
Second Department of Internal Medicine, Kagawa Medical School, Japan.
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MeSH Terms
Benzazepines / pharmacology
Blood Pressure / physiology*
Dopamine / pharmacology,  physiology*
Extracellular Space / physiology
Hypertension / physiopathology
Kidney / innervation,  physiology*
Natriuresis / physiology*
Rats, Inbred Strains
Receptors, Dopamine / drug effects,  physiology
Renal Circulation / physiology
Reg. No./Substance:
0/Benzazepines; 0/Receptors, Dopamine

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