Vasopressin belongs to a family of peptides involved in numerous physiological activities. In the liver vaso-pressin stimulates glycogenolysis, glycolysis and oxygen uptake and increases arterial resistance. All these actions of vasopressin are mediated by V1a receptors and dependent on Ca2+. The increases in cytosolic Ca2+ concentration caused by vasopressin take the form of concentration spikes (oscillations) at subsaturating levels of the hormone. The increased Ca2+ concentrations can also propagate intra- and intercellularly, creating apparent intercellular waves. Such coordinated and sequential signals elicited by vasopressin in the intact perfused liver originate waves of Ca2+ concentration increases running along the hepatocyte plates across the lobules. These waves propagate towards only one direction and coupling between adjacent cells is believed to be provided by gap junctions. Most experimental data indicate that the starting area of the vasopressin-induced Ca2+ concentration waves in the liver lobule is the perivenous zone, where the V1a receptors are more abundant compared to the periportal zone. The higher receptor density in the perivenous zone is the major cause of the perivenous predominance of glycogenolysis stimulation by vasopressin. This predominance, however, seems to exceed the difference in receptor density, the same occurring with the difference in perivenous and periportal initial Ca2+ efflux. Furthermore, at low concentrations, vasopressin stimulates oxygen uptake in the perivenous region, but causes inhibition in the periportal zone. These complexities could be reflecting cell-to-cell interactions via gap junctions and differences between periportal and perivenous cells in the response to the intracellular secondary messengers of vasopressin.
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