Pharmacology

Original Paper

Neural-Renal Interactions in the Hypertension Induced by Papillary Necrosis: Role of Dietary Salt Intake

Dawson, Jr. R. · Wallace D.R.

Author affiliations

Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, Fla., USA

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Pharmacology 1990;40:42–53

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: June 08, 1989
Accepted: September 19, 1989
Published online: June 05, 2008
Issue release date: 1990

Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0

ISSN: 0031-7012 (Print)
eISSN: 1423-0313 (Online)

For additional information: https://www.karger.com/PHA

Abstract

The effects of high salt intake (1.0% NaCl in the drinking water) on rats made hypertensive by 2-bromoethylamine hydrobromide (BEA) treatment (200 mg/kg, i.p.) were examined. BEA-induced medullary necrosis resulted in a mild hypertension (146 ± 5 mm Hg) that was exacerbated by 4 weeks of high salt intake (163 ± 6 mmHg). BEA-treated rats had significant salt-induced increases in urinary norepinephrine excretion and hypothalamic and brainstem norepinephrine content, that were not present in BEA-treated rats drinking tap water or control rats drinking saline. BEA treatment in combination with increased salt intake produced a decrease (p < 0.05) in renal dopamine content and adrenal norepinephrine stores relative to BEA treatment alone. BEA treatment also significantly decreased renal norepinephrine stores and dopamine binding sites irrespective of salt intake. Renal α2-adrenergic receptors and central nervous system stores of dopamine and serotonin were unaffected by BEA treatment. Renal function was well preserved as indicated by normal creatinine, glucose and protein excretion; however, significant (p < 0.05) disruption of the urinary concentrating mechanism was present. These studies suggest that BEA-induced hypertension has a neural component that is exacerbated by high salt intake. The primary defect in BEA hypertension appears to be the lack of circulating antihypertensive lipids that attenuate the ability of salt loads to simulate sympathetic nervous system activity.

© 1990 S. Karger AG, Basel




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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: June 08, 1989
Accepted: September 19, 1989
Published online: June 05, 2008
Issue release date: 1990

Number of Print Pages: 12
Number of Figures: 0
Number of Tables: 0

ISSN: 0031-7012 (Print)
eISSN: 1423-0313 (Online)

For additional information: https://www.karger.com/PHA


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