Evidence in Support of Hypoxia but Against High Potassium and Hyperosmolarity as Possible Mediators of Sustained Vasodilation in Rabbit Cardiac and Skeletal Muscle
The vasoactive properties of hypoxia, elevated extracellular potassium concentration ([K]o), and hyperosmolarity were studied in helical strip preparations of small coronary and deep femoral arteries (260-700 µm, o.d.) equilibrated in a physiological salt solution with an oxygen tension (Po2) of 100 mm Hg, [K]o of 3.18 mM, and an osmolarity of 304 milliosmoles/liter. Increasing [K]o (2-6 mM) or osmolarity (30-50 milliosmoles/liter) produced relaxation of resting tension in 50% of the coronary strips but had no effect on resting tension in deep femoral strips. Sustained increments in [K]o or osmolarity produced concentration-dependent, transient relaxation of aganist-induced contractile tension in both coronary and deep femoral arterial strips: a potassium increment of 4 mM produced 40% relaxation with 100% recovery within 5-6 minutes, an osmotic increment of 30 milliosmoles/liter caused 20-40% relaxation with 100% recovery within 15-60 minutes, and simultaneous potassium (4 mM) and osmotic (30 milliosmoles/liter) increments produced 85-95% relaxation with 100% recovery within 10-15 minutes. Decreasing Po2 from 100 mm Hg to 10 mm Hg resulted in a sustained 35-40% fall in agonist-induced contractile tension. Although a nonspecific additive interaction was observed during a simultaneous change to high [K]o, hyperosmolarity, and hypoxia, for any given level of vascular tone hypoxia had little or no effect on the degree or the duration of the tension relaxation-recovery sequence produced by elevated [K]o, hyperosmolarity, or both. Therefore, it is proposed that hypoxia is the only one of these three factors that, by a direct interaction with vascular smooth muscle cells, can contribute to sustained vasodilation of small arteries in rabbit cardiac or skeletal muscle.
- coronary artery
- local control of blood flow
- physiological salt solution
- deep femoral artery
- Received October 29, 1973.
- Accepted July 15, 1974.
- © 1974 American Heart Association, Inc.