The fish gill is the primary regulatory interface between internal and external milieu and a variety of neurocrine, endocrine, paracrine, and autocrine signals coordinate and control gill functions. Many of these messengers also affect gill vascular resistance, and they, in turn, may be inactivated (or activated) by branchial vessels. Few studies have critically addressed how flow is distributed within the gill filament, the physiological consequences thereof, or the impact of gill hormone metabolism on gill and systemic homeostasis. In most fish, the entire cardiac output perfuses the arterioarterial pathway, and this network probably accounts for the majority of passive- and stimulus-induced changes in vascular resistance. The in-series arrangement of the extensive gill microcirculation with systemic vessels is also indicative of a high capacity for metabolism of plasma-borne messengers as well as xenobiotics. Adenosine, arginine vasotocin (AVT), and endothelin (ET) are the most potent gill constrictors identified to date, and all decrease lamellar perfusion. Perhaps not surprising, they are also inactivated by gill vessels. Acetylcholine favors perfusion of the alamellar filamental vasculature, although the physiological relevance of acetylcholine-mediated responses remains unclear. Angiotensin, bradykinin, urotensin, natriuretic peptides, prostaglandins, and nitric oxide are vasoactive to varying degrees, but their effects on intrafilamental blood flow are unknown. If form befits function, then the complex vascular anatomy of the gill suggests a level of regulatory sophistication unparalleled in other vertebrate organs. Resolution of these issues will be technically challenging but unquestionably rewarding.
Copyright 2002 Wiley-Liss, Inc.