A Ca2+-sensing receptor modulates shark rectal gland function

Abstract

SUMMARY The elasmobranch Squalus acanthias controls plasma osmolality and extracellular fluid volume by secreting a hypertonic fluid from its rectal gland. Because we found a correlation between extracellular Ca2+concentration and changes in cytosolic Ca2+([Ca2+]i), we sought the possible presence of a calcium-sensing receptor in rectal gland artery and tubules. Cytosolic Ca2+ of both tissues responded to the addition of external Ca2+ (0.8-5.3 mmol l-1) in a linear fashion. Spermine,Gd3+ and Ni2+, known agonists of the calcium-sensing receptor, increased [Ca2+]i. To assess the participation of inositol triphosphate (IP3) generation, sarcoplasmic/endoplasmic reticulum (SR/ER) Ca2+ depletion, and activation of store-operated Ca2+ entry, we utilized thapsigargin and ryanodine to deplete Ca2+ SR/ER stores and the inhibitory reagents TMB-8 and 2-APB to block IP3 receptors. In each case, these agents inhibited the[Ca2+]i response to agonist stimulation by approximately 50 %. Blockade of L-channels with nifedipine had no significant effect. Increases in ionic strength are known to inhibit the calcium-sensing receptor. We postulate that the CaSR stimulates Ca2+-mediated constriction of the rectal gland artery and diminishes cyclic AMP-mediated salt secretion in rectal gland tubules during non-feeding conditions. When the shark ingests sea water and fish, an increase in blood and interstitial fluid ionic strength inhibits the activity of the calcium-sensing receptor, relaxing the rectal gland artery and permitting salt secretion by the rectal gland tubules.