Effects of arginine vasopressin and atriopeptin on glial cell volume measured as 3-MG space

Abstract

This study evaluates the hypothesis that arginine vasopressin (AVP) and atriopeptin, peptide hormones synthesized and released within the brain, are regulators of brain cell volume using cultured astroglial cells derived from newborn rats. Cell water content, regarded as volume, was measured in defined, serum-free medium as the 3-O-methylglucose (3-MG) space. Initial experiments established conditions such that glucose, which competes with 3-MG for the glucose carrier, would not interfere with the measurement of the 3-MG space. AVP increased the 3-MG space of glial cells by an average of 25% between 30 and 120 min of exposure, whereas atriopeptin decreased it by 32%. The 3-MG space remained close to normal after coadministration of both peptides. The AVP-dependent increase in 3-MG space was blocked both by the V1 antagonist d(CH2)5Tyr(Me)AVP (Manning compound) and by the cotransport inhibitor, bumetanide. Results are consistent with a role for AVP and atriopeptin in the homeostasis of atroglial cell volume.

Arginine-Vasopressin V1 but not V2 Receptor Antagonism Modulates Infarct Volume, Brain Water Content, and Aquaporin-4 Expression Following Experimental Stroke

“…* P < 0.05 versus saline-treated controls with ischemic stroke [14]. It has previously been demonstrated that ICV administration of AVP significantly increases brain edema after cryogenic injury [50] and following cerebral ischemia [51]. The mechanisms of these set of observations are not fully elucidated at present.…”

Real-Time Monitoring of Changes in Brain Extracellular Sodium and Potassium Concentrations and Intracranial Pressure after Selective Vasopressin-1a Receptor Inhibition following Focal Traumatic Brain Injury in Rats

“…10 The hormone arginine vasopressin (AVP) was identified as a potential mediator of astrocytic cell swelling and subsequent fulminating edematous changes following cerebral injury. [11][12][13][14][15][16][17] It is thought that centrally-released AVP orchestrates the development of brain edema by inducing water and ionic movement. 18,19 Increased AVP levels activate the V1a receptor (V1aR), facilitate water transport across astrocytic cell membranes, and are associated with brain edema formation.…”

Regulation and Function of Cyclic GMP-Mediated Pathways in Glial Cells

“…Although osmotic changes are part of a normal physiological response to maintain brain homeostasis, exaggerated swelling can lead to pathological conditions, for example triggering neuronal damage via the release of glutamate to the extracellular environment. Interestingly, NPs that are known to regulate water and electrolyte content in the brain have been reported to inhibit osmotic swelling in cultured astrocytes [65] and retina Müller cells [66]. Moreover, CNP and cGMP analogues have been shown to decrease intracellular pH in astrocytes by inhibiting a Na + /H + exchanger [67].…”