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Evidence for adrenergic receptor activation in control of hemolymph flow in Procambarus clarkii
Author(s) -
Collett Jason,
Franklin Brandon,
Osborn Jeffrey
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1045.3
Subject(s) - hemolymph , crayfish , vasoconstriction , procambarus clarkii , biology , adrenergic , endocrinology , medicine , anatomy , receptor , ecology
Previous studies suggest decapods have complex neural control of internal organs similar to autonomic control in vertebrates. Norepinephrine (NE) is a key controller of vertebrate cardiovascular function, yet NE regulation of vascular function in decapods remains unclear. This study investigated whether exogenous NE alters hemolymph flow to the tail muscle in freshwater crayfish Procambarus clarkii . It is hypothesized that NE decreases hemolymph flow from adrenergic constriction of the abdominal artery. P. clarkii (25–30g) were obtained from Atchafalay Biological (Raceland, LA) and allowed 2 weeks of environmental acclimation. Crayfish were sedated in an ice bath prior to study. Polyethylene tubing was inserted into the sternal sinus for injections/infusions. A laser Doppler flow probe was placed on the abdominal artery to measure hemolymph flow. NE (30mM) decreased hemolymph flow by 35.2 ± 8.4% (n=8). Co‐infusion of phentolamine (α 1 /α 2 receptor blockade; 5μg/kg/min) abolished NE mediated decreases in hemolymph flow. Stimulation of α 2 receptors with clonidine (10 mM) had no effect on hemolymph flow. Thus, vasoconstriction in P. clarkii may involve α 1 adrenergic mechanisms. Further pharmacological and immunhistochemical experiments will identify specific adrenergic receptor subtypes in the decapod vasculature responsible for vasoconstriction. Supported by NSF #437768 and the Ribble Foundation