Ouabain-resistant hyperpolarization induced by insulin in aggregates of embryonic heart cells

Robert Clark Lantz, L. J. Elsas, R. L. DeHaan

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Spheroidal aggregates formed from trypsin-dissociated 14-day embryonic chicken hearts after 48 hr of rotation on a gyratory shaker. Intracellular recorded resting membrane potentials of aggregates bathed in 1.3 mM K+ balanced salt solution had a mean (±SD) of 64 ± 4 mV. After a stable potential was achieved, addition of 1-100 nM sodium bovine insulin caused a slow hyperpolarization of up to 19mV after 4-5 min, followed in some cases, by a further, more rapid, shift to a potential near E(K). Equivalent hyperpolarizations were observed when insulin was added in the presence of 10 mM ouabain, indicating that enhanced Na+,K+ pump activity was not responsible for the change in membrane potential. The concentration of insulin that produced half-maximal hyperpolarization (2nM) corresponded to the association constant of a high-affinity insulin receptor, suggesting that binding to this class of receptors led to the change in membrane potential. Steady state current-voltage curves from current clamp experiments suggested that insulin produced an increase in slope conductance at potentials near rest by inducing an outward current with an apparent potential negative to -90mV.

Original languageEnglish (US)
Pages (from-to)3062-3066
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume77
Issue number5 I
StatePublished - 1980
Externally publishedYes

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Ouabain
Membrane Potentials
Insulin
Insulin Receptor
Trypsin
Chickens
Salts

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

Ouabain-resistant hyperpolarization induced by insulin in aggregates of embryonic heart cells. / Lantz, Robert Clark; Elsas, L. J.; DeHaan, R. L.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 77, No. 5 I, 1980, p. 3062-3066.

Research output: Contribution to journalArticle

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