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A complex interplay between NO, EDHFs, and KIR channels in cutaneous active vasodilation
Author(s) -
Brunt Vienna E,
Fujii Naoto,
Minson Christopher T
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1133.16
Subject(s) - vasodilation , chemistry , tetraethylammonium , tetraethylammonium chloride , microdialysis , potassium channel , glibenclamide , potassium , pharmacology , medicine , endocrinology , biochemistry , extracellular , organic chemistry , diabetes mellitus
EDHFs contribute largely to skin local hyperemia. We sought to determine if they also contribute to active vasodilation (AVD) during whole‐body heating. Skin blood flow was measured at 4 sites perfused via microdialysis with 1) Lactated Ringer's, 2) tetraethylammonium (TEA, calcium‐sensitive potassium channel & EDHF inhibitor), 3) L‐NAME (NOS inhibitor), and 4) TEA + L‐NAME. Data is presented as % of max cutaneous vascular conductance. TEA had no effect on AVD (plateau at the end of heat stress: control=55.2±4.6% vs. TEA=63.2±5.2%, p=0.34), indicating EDHFs are not obligatory. L‐NAME attenuated plateau (33.7±5.4%); while TEA+L‐NAME augmented plateau compared to L‐NAME alone (49.7±5.3%, p=0.02 vs. L‐NAME), and did not differ from control (p=0.72). From these data, it appears that combined blockade of EDHFs and NOS forces dilation to occur through other means, possibly through inward‐rectifying potassium (K IR ) channels. To test this second hypothesis, we measured AVD at the following sites: 1) Lactated Ringer's, 2) L‐NAME, 3) L‐NAME + TEA, and 4) L‐NAME + TEA + barium chloride (BaCl 2 , K IR channel inhibitor). The addition of BaCl 2 to L‐NAME + TEA reduced plateau to 25.4±6.2% (p=0.01 vs. L‐NAME + TEA), which did not differ from the L‐NAME site (p=0.59). These data combined demonstrate a complex interplay between vasodilatory pathways, with cross talk between NO, EDHFs, and K IR channels. Supported by NIH Grant HL081671