Astrocytes initially swell when exposed to hypotonic medium but rapidly return to normal volume by the process of regulatory volume decrease (RVD). The role that arginine vasopressin (AVP) plays in hypotonically mediated RVD in astrocytes is unknown. This study was therefore designed to determine whether AVP might play a role in astrocyte RVD. With the use of 3-O-[³H]methyl-D-glucose to determine water space, AVP treatment resulted in significantly increased 3-O-methyl-D-glucose water space within 30 s of hypotonic exposure (P = 0.0001) and remained significantly elevated above baseline (1.75 µl/mg protein) at 5 min (P < 0.021). In contrast, in untreated cells, complete RVD was achieved by 5 min. At 30 s, cell volume with AVP treatment was 37% greater than in cells that received no treatment (2.9 vs. 2.26 µl/mg protein, respectively; P < 0.006). The rate of cell volume increase (dV/dt) over 30 s was highly significant (0.038 vs. 0.019 µl · mg protein¹ · s¹ in the AVP-treated vs. untreated group; P = 0.0004 by regression analysis). Additionally, the rate of cell volume decrease over the next 4.5 min was also significantly greater with vasopressin treatment (dV/dt = 0.0027 vs. 0.0013 µl · mg protein¹ · s¹; P = 0.0306). The effect of AVP was concentration dependent with EC₅₀ = 3.5 nM. To determine whether AVP action was receptor mediated, we performed RVD studies in the presence of the V₁-receptor antagonists benzamil and ethylisopropryl amiloride and the V₂-receptor agonist 1-desamino-8-D-arginine vasopressin (DDAVP). Both V₁-receptor antagonists significantly inhibited AVP-mediated volume increase by 40-47% (P < 0.005), whereas DDAVP had no stimulatory effects above control. Taken together, these data suggest that AVP treatment of brain astrocytes in culture appears to increase 3-O-methyl-D-glucose water space during RVD through V₁ receptor-mediated mechanisms. The significance of these findings is presently unclear.

regulatory volume decrease; hypotonicity; V₁-receptor agonist; V₂-receptor agonist

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