Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats

The role of endothelin ETB receptor‐mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension was evaluated using the spotting‐lethal (sl) rat which carries a naturally occurring deletion in the ETB receptor gene. Homozygous (sl/sl) rats treat...

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Veröffentlicht in:British journal of pharmacology 2000-03, Vol.129 (6), p.1060-1062
Hauptverfasser: Matsumura, Yasuo, Kuro, Toshihiko, Konishi, Fumiko, Takaoka, Masanori, Gariepy, Cheryl E, Yanagisawa, Masashi
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container_issue 6
container_start_page 1060
container_title British journal of pharmacology
container_volume 129
creator Matsumura, Yasuo
Kuro, Toshihiko
Konishi, Fumiko
Takaoka, Masanori
Gariepy, Cheryl E
Yanagisawa, Masashi
description The role of endothelin ETB receptor‐mediated action in the development and maintenance of deoxycorticosterone acetate (DOCA)‐salt‐induced hypertension was evaluated using the spotting‐lethal (sl) rat which carries a naturally occurring deletion in the ETB receptor gene. Homozygous (sl/sl) rats treated with DOCA‐salt for 1 week exhibited an earlier onset of hypertension than heterozygous (sl/+) and wild‐type (+/+) rats (systolic blood pressure, SBP; 156.7±3.4 versus 128.8±5.3 and 132.9±3.7 mmHg, respectively). Four weeks after the start of DOCA‐salt treatment, homozygous rats developed marked hypertension, with a SBP of 206.0±4.5 mmHg, compared with 184.8±10.7 mmHg in heterozygous and 164.3±4.8 mmHg in wild‐type rats. Cardiovascular hypertrophy and renal dysfunction observed after 4‐weeks treatment with DOCA‐salt were more severe in homozygous rats, compared to wild‐type and heterozygous animals. These evidences support strongly the view that ETB receptor‐mediated actions are a protective factor in the pathogenesis of DOCA‐salt‐induced hypertension. British Journal of Pharmacology (2000) 129, 1060–1062; doi:10.1038/sj.bjp.0703157
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Homozygous (sl/sl) rats treated with DOCA‐salt for 1 week exhibited an earlier onset of hypertension than heterozygous (sl/+) and wild‐type (+/+) rats (systolic blood pressure, SBP; 156.7±3.4 versus 128.8±5.3 and 132.9±3.7 mmHg, respectively). Four weeks after the start of DOCA‐salt treatment, homozygous rats developed marked hypertension, with a SBP of 206.0±4.5 mmHg, compared with 184.8±10.7 mmHg in heterozygous and 164.3±4.8 mmHg in wild‐type rats. Cardiovascular hypertrophy and renal dysfunction observed after 4‐weeks treatment with DOCA‐salt were more severe in homozygous rats, compared to wild‐type and heterozygous animals. These evidences support strongly the view that ETB receptor‐mediated actions are a protective factor in the pathogenesis of DOCA‐salt‐induced hypertension. 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Neurotransmission. Receptors</topic><topic>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</topic><topic>Pharmacology. 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subjects Biological and medical sciences
deoxycorticosterone acetate‐salt hypertension
endothelin‐1
ETB receptor
Medical sciences
Neuropharmacology
Neurotransmitters. Neurotransmission. Receptors
Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems
Pharmacology. Drug treatments
renal function
Special Reports
title Enhanced blood pressure sensitivity to DOCA‐salt treatment in endothelin ETB receptor‐deficient rats
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