Flux Mediates Stjmulation of Respiratory Activity by Speract in Sea Urchin Spermatozoa"

Speract (Gly-Phe-Asp-Leu-Asn-Gly-Gly-Gly-ValGly), a Tyr analogue ("'yr-Asp-Leu-Asn-Gly-Gly-GlyVal-Gly), carboxyl-terminal fragment (Gly-Gly-GlyVal-Gly), and an NHz-terminaI fragment (Gly-Phe-AspLeu-Asn-Gly-Gly-Gly) were tested for their effects on sea urchin sperm respiration and net H+ efflux. The stimulation of net H' efflux by these peptides was highly correlated with their ability to stimulate cell respiration rates. At an extracellular pH of 6.6, the release of approximately 2.5 ng ions of H'/mg of sperm caused a 1.3 ng atoms of O/min/mg of sperm increase in the respiration rate, independent of the peptide used. As the extracellular pH was raised toward pH 7.5, a much larger stimulation of respiration occurred with a given amount of H+ efflux. The converse was true when the pH was lowered to pH 6.0. Narasin caused a net H+ influx or net H+ efflux dependent on the extracellular pH; respiration rates were increased under conditions of narasin-induced net H+ efflux and were decreased under conditions of net H' Mux. Weak bases (MIS or "is) stimulated sperm respiration, whereas a weak acid (acetic) inhibited sperm respiration rates at constant extracellular pH. Ammonia or speract counteracted the acetic acid inhibition, but speract failed to further stimulate spermatozoa in the presence of ammonia. Raising the extracellular pH also stimulated spermatozoa, and such elevations were shown to increase the intracellular pH. These data suggest that sea urchin sperm respiration rates can be regulated by the intracellular pH and that speract (and analogues) stimulate sperm respiration by primary effects on H' efflux.