Beta-adrenergic-agonist stimulated taurine release from astroglial cells is modulated by extracellular [K+] and osmolarity

Abstract

Astroglial cells are known to release taurine in response to stimulation by a variety of stimuli including beta-adrenergic receptor agonists such as isoproterenol (IPR). The effects of changing osmolarity and extracellular [K+] on IPR-stimulated taurine release were studied with LRM55 cells, a continuous astroglial cell line. IPR-stimulated taurine release decreased almost 8% for each 1% increase in osmolarity, indicating that IPR-stimulated release is highly regulated by the osmolarity of the medium. IPR-stimulated taurine release was greatly enhanced when external [K+] was increased isosmotically by substituting KCl for NaCl but was strongly suppressed when external [K+] was increased hyperosmotically by adding KCl to the medium. Both IPR-stimulated and K(+)-stimulated taurine release depended on external [Cl-]; IPR-stimulated release declined approximately in parallel to K(+)-stimulated release as [Cl-] in the medium was reduced. The high sensitivity of IPR-stimulated release to factors that change cell volume (osmolarity, external [K+], external [Cl-]) is consistent with the idea that IPR, elevated [K+], and reduced osmolarity all elicit taurine release via a single tension-controlled mechanism.