Abstract

Vasopressin, a neurohypophyseal hormone, plays a key role in water balance regulation in mammals. One of the major effects of vasopressin is an increase in the water permeability of collecting duct epithelium, which is based on the cascade of reactions from the membrane receptor of the basolateral membrane to the incorporation of water channels, aquaporins-2, into the apical membrane of the principal cells [1]. The mechanism underlying the involvement of the extracellular matrix, the major component of which is hyaluronan, in the hydroosmotic effect of vasopressin, has been studied the least. Hyaluronan (hyaluronic acid, HA) is a negatively charged nonsulfated linear glycosaminoglycan that is synthesized on the plasma membrane and then translocated through the latter in the form of a growing chain to the extracellular space [2‐4]. In mammalian kidney, HA is distributed heterogeneously: the highest concentration is detected in the medulla, where vasopressin-regulated reabsorption of water takes place [5, 6]. The hypothesis on the role of HA contained in the extracellular matrix in the effect of vasopressin on water transport was first proposed by Ginetzinsky [7]. Later, a negative correlation between the HA content in the renal papilla and the osmolality of excreted urine and a positive correlation between the HA concentration and water content in tissue were found [6, 8]. The possible role of HA as a factor involved in the regulation of hydroosmotic effect of vasopressin stimulates further studies of the mechanisms regulating its metab

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