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1 Department of Pharmacology, University of California, Irvine, Irvine, California, USA
* To whom correspondence should be addressed. E-mail: spduckle{at}uci.edu.
Little is known about vascular effects of testosterone. We previously reported chronic testosterone treatment increases vascular tone in middle cerebral arteries (MCA;
300 µm 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 µm diameter) were isolated from orchiectomized (ORX) and testosterone-treated (ORX+T) rats. Intraluminal
diameters were recorded following step changes in intraluminal pressure (20 - 100 torr)in the absence or presence of NG-nitro-L-arginine-methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor; indomethacin, a cyclooxygenase (COX) inhibitor; and/or apamin and charybdotoxin (CTX), KCa channel blockers used to inhibit endothelial-derived hyperpolarizing factors (EDHF). At intraluminal pressures 
60 torr, arteries from ORX+T developed greater tone as compared to ORX arteries. This difference was abolished by removal of the endothelium but remained after treatment of intact arteries with indomethacin or L-NAME. Additionally, 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. Endothelial removal following 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 endothelial-denuded preparations. In conclusion, testosterone may modulate vascular tone in cerebral arteries by suppressing EDHF.
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