α-Adrenoreceptor influences on liquid movements by in vitro lungs from fetal guinea pigs

Abstract

Doe, S., and A. M. Perks. α-Adrenoreceptor influences on liquid movements by in vitro lungs from fetal guinea pigs. J. Appl. Physiol. 84(2): 746–753, 1998.—Lungs from near-term fetal guinea pigs (60 ± 2 days of gestation) were supported in vitro for 3 h; lung liquid production was monitored by a dye-dilution method. Studies of 30 fetuses showed that untreated preparations produced fluid at 1.34 ± 0.21 ml ⋅ h−1 ⋅ kg body wt−1, but epinephrine at concentrations known at delivery (10−8 and 10−7 M) produced significant reductions or fluid reabsorption (analysis of variance, regression analysis); at high levels (10−6 and 10−5 M), epinephrine had no effect. Maximal responses from 10−7 M epinephrine involved α-adrenoreceptors, since they were abolished by 10−6 M phentolamine (α-antagonist) but were unaffected by 10−6 M propranolol (β-antagonist; n = 36). Activation was through α2-adrenoreceptors, since responses were abolished by 10−4 M yohimbine (α2-antagonist; n = 24) but were resistant to 10−5 M prazosin (α1-antagonist; n = 24). At high levels of epinephrine (10−5 M), where responses did not normally occur, reductions in lung liquid production were large if prazosin was also present ( n = 24), and increases were significant if yohimbine was included ( n = 24). In guinea pigs, epinephrine appears to activate lung fluid reabsorption through α2-adrenoreceptors; at high concentrations only, it can also increase production through α1-adrenoreceptors. Therefore, species differences appear to exist.