Document Detail

Different mechanisms for testosterone-induced relaxation of aorta between normotensive and spontaneously hypertensive rats.
MedLine Citation:
PMID:  10601123     Owner:  NLM     Status:  MEDLINE    
The tension in isolated ring preparations of the thoracic aortae from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) was measured isometrically to study the differences in testosterone-induced relaxation between WKY and SHR aortic rings. Testosterone (9 to 300 micromol/L) induced a concentration-dependent relaxation in both WKY and SHR aortic rings, and the relaxation induced by testosterone was greater in SHR than WKY. The relaxation induced by testosterone was significantly reduced by denudation of endothelium in SHR but not WKY. Indomethacin, an inhibitor of cyclooxygenase, and N(G)-nitro-L-arginine, an inhibitor of nitric oxide (NO) synthase, showed little influence on the relaxation induced by testosterone in both WKY and SHR aortic rings. Glibenclamide, a selective inhibitor of ATP-sensitive potassium channels, significantly reduced the relaxation induced by testosterone in both WKY and SHR aortic rings, although the extent of reduction was greater in WKY than SHR. On the other hand, 4-aminopyridine, a selective inhibitor of voltage-dependent potassium channels, and tetraethylammonium, an inhibitor of calcium-activated potassium channels, significantly reduced the relaxation induced by testosterone in SHR but not WKY. These results suggest that the mechanisms of testosterone-induced vasorelaxation in both WKY and SHR involve, in part, ATP-sensitive potassium channels in the thoracic aortae and that in SHR aortic rings, testosterone may release endothelium-derived substances that may cause hyperpolarization of the cells by a mechanism that involves potassium channels. Moreover, the data show differences between WKY and SHR in the function of ATP-sensitive, voltage-dependent, and calcium-activated potassium channels.
H Honda; T Unemoto; H Kogo
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Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  Hypertension     Volume:  34     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  1999 Dec 
Date Detail:
Created Date:  2000-01-19     Completed Date:  2000-01-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1232-6     Citation Subset:  IM    
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Tokyo, Japan.
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MeSH Terms
4-Aminopyridine / pharmacology
Acetylcholine / metabolism,  pharmacology
Aorta, Thoracic / drug effects,  physiology*
Cyclooxygenase Inhibitors / pharmacology
Dose-Response Relationship, Drug
Glyburide / pharmacology
Hypertension / physiopathology*
Hypoglycemic Agents / pharmacology
Muscle Relaxation / drug effects,  physiology*
Muscle, Smooth, Vascular / drug effects,  physiology*
Nitroarginine / pharmacology
Nitroprusside / pharmacology
Potassium Channels / drug effects,  metabolism
Rats, Inbred SHR
Rats, Inbred WKY
Testosterone / metabolism*,  pharmacology
Tetraethylammonium / pharmacology
Vasodilator Agents / pharmacology
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Hypoglycemic Agents; 0/Potassium Channels; 0/Vasodilator Agents; 10238-21-8/Glyburide; 15078-28-1/Nitroprusside; 2149-70-4/Nitroarginine; 504-24-5/4-Aminopyridine; 51-84-3/Acetylcholine; 58-22-0/Testosterone; 66-40-0/Tetraethylammonium

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