The role of the sodium pump in the control of vascular tone in the rat

Abstract

We studied the effects of failures that alter active Na extrusion on microvascular smooth muscle contraction. As an index of contraction, we measured arterial pressure in perfused isolated rat hindlimbs. The perfusate was oxygenated Krebs-Henseleit solution containing 0-5.9 mM K+, 4% dextran-40, and, in some instances, dog red cells (6-15% hematocrit). The reference solutions contained 5.9 mM K+. Lowering [K+]o by 50%, or more, substantially increased perfusion pressure reversibly; pressure was inversely related to [K+]o. Treatment with 10-3M ouabain, which should completely inhibit Na-K pumps, caused a greater pressure increase than did nominally K+-free media. These effects were observed in the hindlimbs of reserpine-treated (catecholamine-depleted) as well as normal rats and, thus, cannot be explained by modulation of catecholamine release. Perfusion with solutions containing a constant concentration of norepinephrine increased the perfusion pressure with 5.9 mM K present and augmented the responses to both reduced [K+]o and ouabain. The data are discussed in terms of two mechanisms that may lead to a rise in cell Ca2+, and/or (2) the rise in cell Na+, due to Na-K pump inhibition, may cause the fibers to gain Ca2+ by means of Na-Ca exchange.