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Received March 16, 2006
Revised March 31, 2006
Accepted after revision May 21, 2006
1 Univ of Texas Health Science Center
2 University of Texas Health Science Center
* To whom correspondence should be addressed. E-mail: johnson{at}uthscsa.edu.
Cutaneous vascular conductance (CVC) declines in response to local cooling (LC). Previous work indicates that at least part of the vasoconstrictor response to LC may be through an inhibitory effect on nitric oxide synthase (NOS) activity. In this study we further tested that notion. A total of 8 (6 male, 2 female) subjects participated (Part 1 n = 7; Part 2 n = 5, 4 of whom participated in Part 1). Skin blood flow was monitored by laser-Doppler flowmetry. Control of local skin and body temperatures was achieved with Peltier cooler/heater probe holders and water perfused suits, respectively. Microdialysis fibers were inserted aseptically. Saline, L-NAME (20mM), to inhibit NOS activity, and sodium nitroprusside (SNP 10µM) were infused by microdialysis. Bretylium tosylate (BT), to block adrenergic function, was administered by iontophoresis. CVC was calculated from blood flow and blood pressure. In Part 1, the infusion of L-NAME elicited a 35±4% decrease at the L-NAME and BT+L-NAME sites (P < 0.05), subsequent slow LC (34 - 24°C) for 35 min caused a significant (P < 0.05) decrease in CVC at control sites (68±4%) and at the BT treated sites (39±5%). LC caused a further 23±5% of initial baseline decrease in CVC at the L-NAME treated sites (P < 0.05). Importantly, CVC at the BT+L-NAME sites was unaffected by LC (P > 0.05). In Part 2, two sites were pre-treated with both BT and L-NAME. After 50 min, SNP was added as an NO donor to restore baseline CVC at one site. The same LC process as in Part 1 was applied. There was a 24±10% decrease (P < 0.05) in CVC at sites with baseline CVC restored, while, as in Part 1, there was no change (P > 0.05) at sites treated with BT+L-NAME only. These data suggest that the vasoconstriction with slow LC is due to a combination of increased noradrenaline release and decreased activity of both NOS per se and of process(es) downstream of NOS.
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