Abstract

An assessment was made of the relationship between the contractile responses of superfused, helical strips of canine cutaneous and mesenteric arteries and veins and the mechanism by which vasoactive agents initiate an increase in intracellular calcium. Preparations used included mesenteric arteries (0.5-0.8 mm outside diameter), mesenteric veins (0.5-0.8 mm outside diameter), dorsal metatarsal veins (1-2 mm outside diameter) and anterior cranial-tibial arteries (1-2 mm outside diameter). Contractile responses of superfused, helical strips of the aforementioned arteries and veins to norepinephrine, potasssium chloride and barium chloride were recorded. The uptake and distribution of radiocalcium (⁴⁵Ca) in each of the vascular strips were measured in the presence and absence of these vasoactive agents. The experiments were repeated utilizing ruthenium red. an inhibitor of calcium transport. Ruthenium red reduced or abolished contractile responses of all tissues to KCl and BaCl². The contractile responses of superfused tibial and mesenteric arteries and dorsal metatarsal veins to norepinephrine were significantly reduced during superfusion with ruthenium red. Contractile responses of helical strips of mesenteric vein to norepinephrine did not significantly differ before and after superfusion with ruthenium red. Resting tension was unaltered during superfusion with ruthenium red. Norepinephrine increased the uptake of radiocalcium in dorsal metatarsal veins and tibial and mesenteric arteries but not in mesenteric veins. Potassium ion increased the uptake of calcium in all vascular strips studied. Tissues incubated with ruthenium red were unable to accumulate ⁴⁵Ca within the cell. However, ruthenium red did not alter ⁴⁵Ca efflux. These results are consistent with the conclusions that: 1) the responses of dorsal metatarsal veins, anterior mesenteric arteries and anterior tibial arteries to norepinephrine were mediated by an increase in membrane permeability to calcium and by release of calcium from intracellular sites: 2) the contractile response of anterior mesenteric veins to norepinephrine is primarily not mediated by an increase in membrane permeability to calcium ions; 3) the contractile response of anterior mesenteric veins to norepinephrine is primarily mediated by release of calcium from intracellular binding sites; and 4) resting tension is not directly dependent on extracellular calcium concentration.