Abstract

Salt may have a direct effect on vascular function by reducing nitric oxide (NO) production.PURPOSEThe purpose of this study was to examine the effects of hypertonic saline on NO‐mediated cutaneous vasodilation in response to local heating.METHODSNine healthy subjects (23 ± 2 years) were studied. We measured cutaneous red blood cell flux via laser Doppler in conjunction with intradermal microdialysis of 1) Ringer's solution (R), 2) 0.9% normal saline (NS), 3) 3% hypertonic saline (HS), and 4) 10 mM NG‐nitro‐L‐arginine methyl ester (L‐NAME) during local heating to 42°C. Microdialysis of 28 mM sodium nitroprusside (SNP) at 43°C was used for assessment of maximum cutaneous vascular conductance (CVCmax) and data was expressed as a percentage of CVCmax (%CVCmax).RESULTSBaseline %CVCmax did not differ between the four microdialysis sites (HS: 9 ± 4, R: 11 ± 6, NS: 7 ± 4, L‐NAME: 7 ± 2%; p = 0.9). Hypertonic saline significantly attenuated the plateau %CVCmax compared to Ringer's and 0.9% normal saline (HS: 74 ± 12, R: 89 ± 4, NS: 89 ± 5%; p< 0.01) and L‐NAME reduced the plateau %CVCmax compared to other three sites (47 ± 7%, p< 0.01).CONCLUSIONHypertonic saline attenuates the cutaneous vasodilation response to local heating suggesting a direct effect of salt on microvascular function. This effect may be mediated through a decreased production and/or availability of NO.Supported by Grant DK080469.

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