NEUROPARSINS INDUCE PHOSPHOINOSITIDE BREAKDOWN IN THE MIGRATORY LOCUST RECTAL CELLS

1. 1. Neuroparsin (Nps) antidiuretic (AD) signal transduction in migratory locust rectal cells is mediated by phosphoinositide turnover and calcium ion (Ca2+). 2. 2. Using the suitable biological in-vitro assay of everted rectum and selective stimulators of protein kinase C (PKC), 1-stearoyl-2-arachidonoyl-sn-glycerol (SAG) and active phorbol ester tumor promotor or phorbol-12-myristate-13-acetate (PMA), we provoked an increase of fluid reasorption, while polymyxin B (PKC inhibitor) abolished Nps, SAG or PMA induced AD processes. Myoinositol (MI) as well as an intracellular Ca2+ increase obtained with the use of both Ca2+ ionophores A23187 and ionomycin stimulated fluid reabsorption, as Nps do. 3. 3. Lithium (as lithium chloride) blocked entirely the AD effects of Nps. while it inhibited partially the AD actions of MI and SAG. 4. 4. The level of lithium action was discussed, and participation of an inositol trisphosphate was formulated as an hypothesis. 5. 5. Stimulation of the phosphoinositide turnover following transduction of the Np AD signal caused a simultaneous inhibition of two other second messenger systems previously found in the migratory locust rectal cells: cyclic adenosine monophosphate (cAMP) mediating AD signal generated by a factor from the glandular lobes of the corpora cardiaca, and cyclic guanosine monophosphate (cGMP) supposed to be located in rectal muscular cells. 6. 6. The respective decreases of cAMP and cGMP were due probably to an activation of the cyclic nucleotide dependent phosphodiesterases by Ca2+. 7. 7. The data are consistent with an important role of PKC and Ca2+ in modulating the AD responses of insect rectal cells, and a scheme on possible ways followed in transduction of the AD signals was proposed as a working hypothesis. © 1989.