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Effects of the beta‐adrenergic agonist, ritodrine, and insulin on plasma potassium concentrations in fetal lambs
Author(s) -
Bassett JM,
Bomford J,
Hanson C,
Mott JC,
Weeding CM
Publication year - 1992
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1992.sp003626
Subject(s) - ritodrine , endocrinology , medicine , fetus , agonist , insulin , alpha (finance) , beta (programming language) , chemistry , receptor , pregnancy , gestation , biology , construct validity , genetics , nursing , computer science , patient satisfaction , programming language
Prolonged infusion of the beta 2‐adrenergic agonist, ritodrine, into sheep during late pregnancy decreased maternal plasma K+ from 3.6 to 2.5 mmol l‐1 during the first 6‐8 h of infusion, as it does during tocolysis in women. This decrease was not accompanied by significant change in fetal plasma K+ concentration. Ritodrine infusion (1‐3.5 micrograms kg‐1 min‐1) directly into the fetus also did not decrease fetal plasma K+ significantly. In contrast, insulin (2.5 mU kg‐1 min‐1), infused together with glucose (3.6 mg kg‐1 min‐1) directly into the fetus decreased fetal plasma K+ concentration by 0.8 mmol l‐1 within 1 h. The results suggest immaturity in beta 2‐adrenergic receptor regulation of electrogenic K+ uptake by muscle in fetal lambs.