caa a22 4500 475833090 CHVBK 20180406123846.0 cr unu---uuuuu 170329e20000201xx s 000 0 eng 10.1023/A:1007835003493 doi (NATIONALLICENCE)springer-10.1023/A:1007835003493 Vascular ATP-Dependent Potassium Channels, Nitric Oxide, and Human Forearm Reactive Hyperemia [Elektronische Daten] [Alan Bank, Ron Sih, Kathleen Mullen, Michael Osayamwen, Paul Lee] Vascular ATP-dependent potassium (K+ ATP) channels open and contribute to reactive hyperemia (RH) in animals. The contribution of K+ ATP channels to ischemic vasolidation during RH and interactions with endothelium-derived nitric oxide have not been well characterized in human subjects. RH blood flow responses (mL/dL) following 5 minutes of cuff occlusion were measured using strain-gauge plethysmography in 22 normal human subjects age 42 ± 2 years. Measurements were obtained at baseline and following intra-arterial administration of the K+ ATP channel closer glibenclamide, the nitric oxide synthase inhibitor L-N-monomethyl arginine (L-NMMA), or both drugs simultaneously. Glibenclamide (100 µg/min) did not change basal flow (2.7 ± 0.3 to 2.7 ± 0.3 mL/min/dL), but L-NMMA (8 µmol/min) and combined glibenclamide and L-NMMA significantly (p < 0.05) decreased basal flow (3.0 ± 0.5 to 2.0 ± 0.2 and 3.3 ± 0.5 to 2.5 ± 0.3, respectively). Glibenclamide significantly (p < 0.01) decreased RH flow (18.2 ± 1.3 to 14.8 ± 1.3) and excess flow (5.3 ± 1.2 to 1.3 ± 1.3). L-NMMA significantly (p < 0.05) decreased RH flow (21.2 ± 1.8 to 18.9 ± 1.9) and tended to decrease excess flow (6.1 ± 2.2 to 3.9 ± 2.5). Combined drug infusion significantly (p < 0.1) decreased RH flow (21.6 ± 2.2 to 18.0 ± 2.4) and excess flow (6.3 ± 1.6 to 1.6 ± 1.6), with reductions in RH and excess flow similar to those following glibenclamide infusion alone. We conclude that forearm vascular K+ ATP channels are closed at baseline. They open and contribute to RH vasodilation. The addition of nitric oxide inhibition to K+ ATP channel blockade does not result in additive or synergistic inhibition of RH. Kluwer Academic Publishers, 2000 potassium channels nationallicence endothelium-derived factors nationallicence vasolidation nationallicence blood flow nationallicence Bank Alan Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut Sih Ron Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut Mullen Kathleen Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut Osayamwen Michael Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut Lee Paul Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut Cardiovascular Drugs and Therapy Kluwer Academic Publishers 14/1(2000-02-01), 23-29 0920-3206 14:1<23 2000 14 10557 https://doi.org/10.1023/A:1007835003493 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1023/A:1007835003493 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Bank Alan Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut NATIONALLICENCE 700 1- Sih Ron Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut NATIONALLICENCE 700 1- Mullen Kathleen Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut NATIONALLICENCE 700 1- Osayamwen Michael Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut NATIONALLICENCE 700 1- Lee Paul Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota aut NATIONALLICENCE 773 0- Cardiovascular Drugs and Therapy Kluwer Academic Publishers 14/1(2000-02-01), 23-29 0920-3206 14:1<23 2000 14 10557 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer