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Bivalve culture is know to affect some interactions between the water column and the benthic environment with the organic enrichment. An in situ mesocosms experiment was used to determine the influence of mussel biodeposition on the benthic ecosystem in St. Peters Bay, Prince Edward Island, eastern Canada. Eight mussel densities (0 to 2266 mussels m-2) were placed above mesocosms to reproduce the organic enrichment from a mussel farm over 12 weeks. The experimental procedure created an accumulation of organic matter on the seafloor with increasing mussel densities. Some benthic parameters had the predicted response to organic enrichment, with the presence of anoxic sediment in sediment profile images, increased water and organic matter content, and reduced infaunal abundance and species richness. Other parameters, including redox potential, total free sulfides, and the response of the biotic index AMBI, had inconsistent responses to mussel biodeposition-related organic enrichment. Given that other studies done in other locations have observed varying results, results suggest that measurement of various parameters is important to interpret the influence of deposition from mussel farms. The conditions of the site and the study duration are also parameters to consider when evaluating the results from mesocosm studies. Results from this study also suggest that St. Peters Bay is likely impacted by biodeposition from the mussels farmed there. [ABSTRACT FROM AUTHOR]

Objective: Peroxisome proliferator-activated receptors (PPARs) may modulate in vitro the vascular production of vasoactive peptides such as endothelin-1 (ET-1). Thus, we investigated in vivo the interaction between PPARs and ET-1 in deoxycorticosterone acetate (DOCA)-salt rats that overexpress vascular ET-1., Methods and Results: Unilaterally nephrectomized 16-week-old Sprague-Dawley rats (Uni-Nx) were divided into 4 groups (n=6 each): control group, DOCA-salt group, DOCA-salt+PPAR-gamma activator (rosiglitazone, 5 mg x kg(-1) x d(-1)), or DOCA-salt+PPAR-alpha activator (fenofibrate, 100 mg x kg(-1) x d(-1)). Systolic blood pressure was significantly increased in the DOCA-salt group (240+/-11 vs 121+/-2 mm Hg in Uni-Nx, P<0.01). Progression of hypertension was partially prevented by coadministration of rosiglitazone (172+/-3 mm Hg vs DOCA-salt, P<0.05) but not by fenofibrate. Both PPAR activators abrogated the increase in prepro-ET-1 mRNA content in the mesenteric vasculature of DOCA-salt rats. The media-to-lumen ratio was increased in DOCA-salt rats (10.3+/-0.9% vs 4.9+/-0.5% in Uni-Nx rats, P<0.01). Rosiglitazone and fenofibrate prevented the hypertrophic remodeling observed in DOCA-salt rats without affecting vascular stiffness. Rosiglitazone but not fenofibrate prevented endothelial dysfunction in pressurized mesenteric arteries. Finally, both rosiglitazone and fenofibrate prevented the vascular increase in superoxide anion production induced in DOCA-salt animals., Conclusions: PPAR-alpha and -gamma activators were able to modulate endogenous production of ET-1 and had beneficial vascular effects in endothelin-dependent hypertension.