Pacific hagfish (Eptatretus stoutii) slime mucin vesicles are released by holocrine secretion with membranes that remain intact until the vesicle contacts seawater and ruptures. This thesis is an investigation of the mechanisms that drive mucin vesicle rupture for mucin release. Using isolated mucin vesicles collected from the slime glands of the hagfish, I tested the effects of a variety of solutions and drugs on vesicle rupture. I found that there are two categories of mucin vesicle that differ in their sensitivity to calcium ions, and that calcium-dependent vesicle rupture was inhibited with anion channel inhibitors. I also found that vesicle swelling rate was reduced by the aquaporin inhibitor mercuric chloride. Together, these data suggest that mucin vesicle rupture is partially dependent on the movement of chloride ions from seawater through calcium-activated anion channels and the rapid influx of water through aquaporin-like proteins in the vesicle membrane. / NSERC Discovery Grant, NSERC CGSM scholarship, Canada Foundation for Innovation, Ontario Ministry of Research and Innovation