Document Detail

Testosterone suppresses endothelium-dependent dilation of rat middle cerebral arteries.
MedLine Citation:
PMID:  14551047     Owner:  NLM     Status:  MEDLINE    
Little is known about vascular effects of testosterone. We previously reported chronic testosterone treatment increases vascular tone in middle cerebral arteries (MCA; 300 microm diameter) of male rats. In the present study, we investigated the hypothesis that physiological levels of circulating testosterone affect endothelial factors that modulate cerebrovascular reactivity. Small branches of MCA (150 microm diameter) were isolated from orchiectomized (ORX) and testosterone-treated (ORX+T) rats. Intraluminal diameters were recorded after step changes in intraluminal pressure (20-100 Torr) in the absence or presence of N(G)-nitro-L-arginine-methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor; indomethacin, a cyclooxygenase (COX) inhibitor; and/or apamin and charybdotoxin (CTX); and K(Ca) channel blockers used to inhibit endothelium-derived hyperpolarizing factors (EDHF). At intraluminal pressures >or=60 Torr, arteries from ORX+T developed greater tone compared with ORX arteries. This difference was abolished by removal of the endothelium but remained after treatment of intact arteries with indomethacin or L-NAME. In addition, testosterone treatment had no effect on cerebrovascular production of endothelin-1 or prostacyclin nor did it alter protein levels of endothelial NOS or COX-1. Endothelium removal after L-NAME/indomethacin exposure caused an additional increase in tone. Interestingly, the latter effect was smaller in arteries from ORX+T, suggesting testosterone affects endothelial vasodilators that are independent of NOS and COX. Apamin/CTX, in the presence of L-NAME/indomethacin, abolished the difference in tone between ORX and ORX+T and resulted in vessel diameters similar to those of endothelium-denuded preparations. In conclusion, testosterone may modulate vascular tone in cerebral arteries by suppressing EDHF.
Rayna J Gonzales; Diana N Krause; Sue P Duckles
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2003-10-09
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  286     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-01-12     Completed Date:  2004-03-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H552-60     Citation Subset:  IM    
Department of Pharmacology, College of Medicine, University of California, Irvine 92697-4625, USA.
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MeSH Terms
Apamin / pharmacology
Body Weight
Charybdotoxin / pharmacology
Cyclooxygenase 1
Cyclooxygenase Inhibitors / pharmacology
Endothelium, Vascular / drug effects,  physiology*
Indomethacin / pharmacology
Isoenzymes / metabolism
Membrane Proteins
Middle Cerebral Artery / drug effects,  physiology*
Muscle Tonus
Muscle, Smooth, Vascular / drug effects,  physiology*
NG-Nitroarginine Methyl Ester / pharmacology
Prostaglandin-Endoperoxide Synthases / metabolism
Rats, Inbred F344
Testosterone / blood,  pharmacology*
Vasodilation / drug effects*
Grant Support
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Isoenzymes; 0/Membrane Proteins; 115422-61-2/Charybdotoxin; 24345-16-2/Apamin; 50903-99-6/NG-Nitroarginine Methyl Ester; 53-86-1/Indomethacin; 58-22-0/Testosterone; EC 1; EC Synthases; EC protein, rat

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