This study analyzes the mechanisms involved in the responses to ouabain in cat cerebral and femoral arteries and characterizes the electrogenic Na+ pump present in these vessels. The latter was accomplished by measurement of [3H]-ouabain binding to arterial membrane fractions, K+-elicited relaxation and ouabain-sensitive 86Rb+ uptake. 2. Ouabain induced transient contraction in cylindrical segments of cerebral arteries. This contraction was reduced by verapamil (3 X 10(-6) M) and Ca2+-removal from the medium but was not modified by phentolamine (3 X 10(-6) M) or pretreatment with reserpine. However, the contraction elicited by ouabain in femoral artery segments lasted longer, and was reduced by Ca2+-omission, phentolamine or reserpine, but remained unaffected by verapamil. 3. The immersion of the arteries in low-Na+ (25 mM) medium abolished the contraction caused by ouabain. 4. The exposure of the arteries to a K+-free medium induced a small transient increase in tension, and the subsequent application of K+ (7.5 mM) elicited a marked relaxation. This effect was greater in cerebral than in peripheral arteries, and was suppressed by ouabain (10(-4) M). 5. Scatchard analysis of the [3H]-ouabain binding to arterial membrane fractions suggested a single class of binding sites. The KD values for both kinds of arteries were of similar order, while the Bmax value was greater in cerebral than in femoral arteries. 6. Total and ouabain-sensitive 86Rb+ uptakes were greater in cerebral than in femoral vessels. 7. These results indicate that: (1) ouabain-induced contraction of cerebral arteries is due to a direct effect on vascular smooth muscle cells, while in femoral arteries it is due to noradrenaline release from adrenergic nerve terminals; and (2) the electrogenic Na+ pump activity is greater in cerebral than in peripheral arteries.
