Individualities in post-serotonin attenuation and Na+/K+ pump activity in vascular smooth muscle

Prior treatment with serotonin (10(-8)-10(-7) M for 6 min) attenuated responses of rabbit mesenteric arteries to norepinephrine (NE) by 18-62%, but was without effect on the responses of the rabbit aorta. K+ relaxation responses in the mesenteric arteries were enhanced by serotonin, but in the aortic strips K+ relaxation occurred either before or after treatment with serotonin. Maximum relaxation to monensin was similar in the two tissues. Post-serotonin attenuation and K+ and monensin relaxation were blocked by ouabain, indicating that they depended on Na+/K+ pump stimulation. Intracellular Na+ contents (Nai) were determined in the vessels by the Li substitution method. Nai was greater, and was increased to a greater extent by serotonin and K(+)-free physiological salt solution in the mesenteric artery compared to the aorta, suggesting that the cell membrane of the mesenteric artery is leakier to Na+ than is that of the aorta. We conclude that the absence of post-serotonin attenuation in the aorta results from the failure of serotonin to increase Nai and thereby to stimulate the Na+/K+ pump in this tissue. This study demonstrates that important individualities in vascular smooth muscle reactivity even in the same animal may result from differences in membrane permeability to sodium.