Mechanisms of subcellular cytosolic Ca2+ signaling evoked by stimulation of the vasopressin V1a receptor

• Published in: The Journal of biological chemistry 1992-11, Vol.267 (32), p.23282-23289
• Main Authors: NATHANSON, M. H, MOYER, M. S, BURGSTAHLER, A. D, O'CARROLL, A.-M, BROWNSTEIN, M. J, LOLAIT, S. J
• Format: Article
• Language: English
• Subjects: Animals; Arginine Vasopressin - metabolism; Arginine Vasopressin - pharmacology; Biological and medical sciences; Caffeine - pharmacology; Calcium - metabolism; Cell Membrane - drug effects; Cell Membrane - physiology; Cell physiology; Cloning, Molecular; Cytosol - metabolism; Female; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Inositol 1,4,5-Trisphosphate - pharmacology; Ionomycin - pharmacology; Kinetics; Microscopy, Fluorescence; Molecular and cellular biology; Oocytes - drug effects; Oocytes - physiology; Receptors, Vasopressin - drug effects; Receptors, Vasopressin - genetics; Receptors, Vasopressin - physiology; Recombinant Proteins - drug effects; Recombinant Proteins - metabolism; Signal Transduction; Time Factors; Xenopus
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/s0021-9258(18)50088-0

Receptor activation may result in distinct subcellular patterns of Ca2+ release. To define the subcellular distribution of Ca2+i signals induced by stimulation of the vasopressin V1a receptor, we expressed the cloned receptor in Xenopus oocytes. Oocytes were then loaded with fluo-3 and observed using confocal microscopy. Vasopressin induced a single concentric wave of increased Ca2+ that radiated inward from the plasma membrane. With submaximal stimulation, however, regions of the Ca2+ wave spontaneously reorganized into repetitive (oscillatory) waves. Focal stimulation of a small part of the plasma membrane resulted in a Ca2+ wave which began at the point of stimulation, radiated toward the center of the cell, then reorganized into multiple foci of repetitive, colliding waves and spirals of increased Ca2+i. The pattern of Ca2+ signaling induced by focal or global stimulation was not altered in Ca(2+)-free medium, although signals did not propagate as fast. Finally, subcellular Ca2+ signaling patterns induced by vasopressin were inhibited by caffeine, while neither vasopressin nor microinjection of inositol trisphosphate blocked caffeine-induced increases in cytosolic Ca2+. Thus, stimulation of the V1a receptor in this cell system induces a complex pattern of Ca2+ signaling which is influenced by (1) the magnitude of the stimulus, (2) the distribution of the surface receptors that are stimulated, and (3) mobilization of Ca2+ from the extracellular space as well as from two distinct endogenous Ca2+ pools. The manner in which a single type of receptor is activated may represent an important potential mechanism for subcellular Ca2+i signaling.