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1. In the first part of this investigation we studied the experimental conditions under which the 'lanthanum method' gives valid estimations of the changes in intracellular calcium induced by either tetraethylammonium chloride (TEA) or high K in the rabbit main pulmonary artery. Subsequently, the effect of TEA on Ca movements in this blood vessel was measured. 2. The uptake of 140La by the vascular tissue is time- and concentration-dependent; it is separated into an early and a late phase. La binds to at least two classes of extracellular sites with affinities of 0.06 and 4.76 M. 3. A 1 hr exposure of the vascular strips to a 1 mM-La solution appears to be a convenient treatment for removal of Ca from the extracellular space. Under these conditions (a) 45Ca efflux from an intracellular compartment loaded with Ca during exposure to TEA or K is virtually blocked, (b) there is no major penetration of La into the smooth muscle cells as revealed by electron microscopy, and (c) there is no change in the size of the extracellular space. 4. TEA increases in a concentration-dependent manner the La-resistant 45Ca content (maximum increase 0.18 m-mole 45Ca/kg wet weight in response to 70 mM-TEA). There is a linear relationship between log concentration TEA and 45Ca influx. 5. The calcium antagonist verapamil (10(-6) and 10(-5) M) inhibits the TEA-induced 45Ca influx. 6. The increase in 45Ca influx produced by K (20 or 30 mM) is markedly enhanced by TEA. 7. The noradrenaline-induced increase in 45Ca accumulation is not influenced by TEA. 8. 45Ca efflux from the La-resistant Ca space is increased by TEA both in the presence and in the absence of non-radioactive Ca in the medium. 9. It is concluded that TEA contracts the vascular smooth muscle cells of the rabbit main pulmonary artery by an increase in the Ca permeability of the cell membrane.