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INTEGRATIVE |
The Pennsylvania State University, Noll Laboratory,
1 Department of Kinesiology
2 Graduate Physiology Program, University Park, PA 16802, USA
Reflex cutaneous vasodilatation is dependent on nitric oxide (NO), which is diminished in hypertension (HTN). Arginase may be up-regulated with HTN, which preferentially metabolizes L-arginine (L-arg), competing with NO-synthase (NOS)-mediated pathways and limiting NO synthesis. We hypothesized that NO-dependent vasodilatation would be attenuated in HTN skin, and arginase inhibition (A-I) alone or with concurrent L-arginine supplementation, would augment vasodilatation. Five microdialysis fibres were placed in skin of eight unmedicated subjects with HTN (mean arterial pressure (MAP), 112 ± 1 mmHg) and nine age-matched normotensive (AMN) (MAP: 87 ± 1 mmHg) men and women to serve as: control (C, Ringer solution), NOS inhibited (NOS-I, 10 mM L-NAME), A-I (5 mM BEC + 5 mM nor-NOHA), L-arg supplemented (L-arg, 10 mM L-arg), and combined A-I +
L-arg. Reflex vasodilatation was induced by using a water-perfused suit to increase oral temperature (Tor) 1.0°C. Red cell flux was measured by laser-Doppler flowmetry over each site. Cutaneous vascular conductance was calculated (CVC = flux/MAP) and normalized to maximal CVC (28 mM SNP + local heating to 43°C). The 
%CVCmax between the control and NOS-I site was calculated as the difference between C and NOS-I sites. Maximal CVC was attenuated in the HTN subjects by 
25% compared with AMN subjects (P < 0.001). Throughout, whole body heating %CVCmax was not different between the groups (HTN, 43 ± 3%CVCmax
versus AMN, 45 ± 3%CVCmax, P > 0.05). NOS-I significantly decreased %CVCmax in both groups but %CVCmax was greater in the HTN group (HTN, 32 ± 4%CVCmax
versus AMN, 23 ± 3%CVCmax, P < 0.05). The %CVCmax between the control and NOS-I sites was attenuated at Tor > 0.5°C in the HTN group (P < 0.001 versus AMN). A-I alone augmented %CVCmax only in the HTN group (HTN, 65 ± 5%CVCmax
versus AMN, 48 ± 3%CVCmax, P < 0.05). L-Arg alone did not affect %CVCmax in either group (HTN, 49 ± 5%CVCmax
versus AMN, 49 ± 3%CVCmax, P > 0.05). Combined A-I +
L-arg augmented %CVCmax in both subject groups compared with their respective control sites (HTN, 60 ± 7%CVCmax
versus AMN, 61 ± 3%CVCmax, both P < 0.05 versus respective control sites). Vasodilatation is attenuated with HTN due to decreased NO-dependent vasodilatation and can be augmented with arginase inhibition but not L-arg supplementation, suggesting that arginase is up-regulated with HTN.
(Received 23 January 2007;
accepted after revision 1 March 2007;
first published online 8 March 2007)
Corresponding author L. A. Holowatz: 123 Noll Laboratory, University Park, PA 16802, USA. Email lma191{at}psu.edu
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