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Leg exercise hyperemia: role of nitric oxide synthase and cyclooxygenase
Author(s) -
Limberg Jacqueline K,
Schrage William G,
Wilkins Brad W,
Johnson Christopher P,
John Eisenach,
Dietz Niki M,
Curry Timothy B,
Joyner Michael J
Publication year - 2008
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.22.1_supplement.1237.3
Subject(s) - medicine , vasodilation , heart rate , anesthesia , cyclooxygenase , reactive hyperemia , nitric oxide synthase , blood pressure , cardiology , nitric oxide , blood flow , oxygen saturation , oxygen , chemistry , biochemistry , enzyme , organic chemistry
The key vascular signals regulating muscle blood flow during exercise are unclear. We tested the hypothesis that in young adults, leg blood flow (LBF) during exercise would be reduced independently by pharmacological inhibition of nitric oxide synthase (NOS) and cyclooxygenase (COX). In 13 young adults, we measured heart rate (ECG), blood pressure (femoral artery and vein), blood gases, and venous oxygen saturation (indwelling oximeter) during steady‐state dynamic (60/min) knee extension exercise. LBF was determined by Doppler ultrasound of the femoral artery. Exercise (20W) increased leg vascular conductance (LVC) from 4± 1 to 33± 3 ml/min/100mmHg. The NOS inhibitor L‐NAME reduced LVC by ∼10% to 30± 1. Infusion of the COX inhibitor, ketoralac (n=9), increased LVC from 30± 1 to 34± 2. L‐NAME infusion reduced venous oxygen saturation from 48 to 38%, suggesting greater extraction to maintain oxygen consumption. Control intra‐arterial infusions of acetylcholine (ACH) and nitroprusside (NTP) tested inhibitor efficacy. The change in LVC to two doses of ACh was blunted 53 and 15%, by L‐NAME+ketorolac infusion. In contrast, the LVC responses to NTP were unaltered. These data implicate a modest role for NO‐mediated leg exercise hyperemia in adults and a potentially modest LBF restraint by vasoconstrictor prostaglandins. Funded by the NIH HL‐46493 and the Minnesota Obesity Center.