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SYNOPSIS. Many xenobiotic compounds introduced into the environment by human activity have been shownto adversely affect wildlife. Reproductive disorders in wildlife include altered fertility, reduced viability of offspring, impaired hormone secretion or activity and modified reproductive anatomy. It has been hypothesized that many of these alterations in reproductive function are due to the endocrine disruptive effects of various environmental contaminants. The endocrine system exhibits an organizational effect on the developing embryo. Thus, a disruption of the normal hormonal signals can permanently modify the organization and future function of the reproductive system. We have examined the reproductive and developmental endocrinology of several populations of American alligator (Alligator mississippiensis) living in contaminated and reference lakes and used this species as a sentinel species in field studies. We have observed that neonatal and juvenile alligators living in pesticide-contaminated lakes have altered plasma hormone concentrations, reproductive tract anatomy and hepatic functioning. Experimental studies exposing developing embryos to various persistent and nonpersistent pesticides, have produced alterations in gonadal steroidogenesis, secondary sex characteristics and gonadal anatomy. These experimental studies have begun to provide the causal relationships between embryonic pesticide exposure and reproductive abnormalities that have been lacking in pure field studies of wild populations. An understanding of the developmental consequences of endocrine disruption in wildlife can lead to new indicators of exposure and a better understanding of the most sensitive life stages and the consequences of exposure during these periods.

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In mammals, the vascular endothelium releases a variety of paracrine factors, including the vasodilatory prostaglandin (PG)I2 and nitric oxide (NO), which is generally accepted as the major endothelium-derived relaxing factor (EDRF) in mammals. Current evidence for the vascular NO-EDRF system in fishes is contradictory. In addition, the role of PGs in the control of fish vascular tension is also unclear. We have utilized isolated rings of the ventral aorta of the spiny dogfish shark to examine the ability of various components of the NO system to dilate this vessel. Neither the NO precursorl-arginine, the NO donor sodium nitroprusside, nor NO itself dilated the rings. The Ca2+ ionophore A-23187 did produce an endothelium-dependent dilation that was not inhibited by the NO synthase inhibitor N G-nitro-l-arginine methyl ester but was inhibited by the cyclooxygenase inhibitor indomethacin, suggesting that PGs are involved. PGE1 and carbaprostacyclin, but not PGI2, produced concentration-dependent dilation, and intact aortic rings secreted five times as much PGI2as PGE in both the unstimulated state and after stimulation with A-23187. Our data suggest strongly that a PG, most probably PGI2, is the EDRF in the ventral aorta of this shark species.