Effects of hypoxia on isolated vessels and perfused gills of rainbow trout

Local hypoxia dilates systemic and constricts pulmonary blood vessels in ma mmals without neural or humoral involvement. The direct effects of hypoxia on isolated vessels from bony fish have not been examined. In the present s tudy, isolated vessels (efferent branchial artery, EBA; coeliacomesenteric artery, CMA; ventral aorta, VA; and anterior cardinal vein, ACV) from rainb ow or steelhead trout (Oncorhynchus mykiss) were subjected to either passiv e load (resting tension) or contracted with a ligand or 50 mM KCI and then subjected to 60 min of hypoxia by N-2 administration and an additional 30 m in of normoxia. All vessels were usually refractory to hypoxia under condit ions of resting tension. EBAs, CMAs and VAs pre-contracted with a receptor- mediated ligand were all significantly relaxed by hypoxia and only VAs reco vered significantly upon subsequent restoration of normoxia. In contrast, t ension in all arteries pre-contracted with 50 mM KCI was elevated further i n response to hypoxia. Conversely, ligand-contracted ACVs responded to hypo xia with a further increase in tension, whereas KCI-contracted ACVs relaxed . During apparently random 2-3-week periods EBA and CMA from steelhead and EBA from rainbow trout were hyper-reactive to hypoxia. Steelhead vessels re sponded to hypoxia. with a rapid contraction that increased in magnitude ov er 3 days. These contractions were independent of pre-stimulation and they were dose-dependent upon PO2. In isolated gills, hypoxic perfusate produced an immediate but transient elevation of resistance (R-GILL) in all four gi ll arches. R-GILL increased by as much as 30% of initial values and this re sponse was unaltered upon a second hypoxic exposure. These studies demonstr ate that isolated vascular segments of rainbow trout are indeed responsive to hypoxia and that these differential responses are vessel and tone depend ent and the overall response may be altered by as yet unknown seasonal or e nvironmental factors. Hypoxia-induced arterial relaxation is blocked by ele vated external [K+], implicating alteration of transmembrane K+ conductance and/or membrane potential in this depressor response. K+-channel closure o r voltage-gated Ca2+ influx cannot account for arterial vasoconstriction du e to hypoxia during KCl+ contractions. Vascular Vascular responses to hypox ia could have a profound impact on local flow in vivo and could mediate ven tilation-perfusion matching in the branchial circulation of fish. (C) 2001 Elsevier Science Inc. All rights reserved.