Adrenergic inhibition of carbon dioxide excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange.

S. F. Perry, C. M. Wood, S. Thomas, P. J. Walsh

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

We have used a sensitive new technique to assess the mechanism(s) of adrenergic inhibition of rainbow trout (Oncorhynchus mykiss) red blood cell (RBC) carbon dioxide excretion in vitro. The effect was only apparent using blood acidified to simulate metabolic acidosis. Red blood cell CO2 excretion was inhibited in a dose-dependent manner by physiologically relevant concentrations of noradrenaline (10-1000 nmol l-1) or adrenaline (100-1000 nmol l-1). The beta-adrenoceptor antagonist propranolol abolished the inhibitory effect of adrenaline, whereas the alpha-adrenoceptor antagonist phentolamine was without effect. The action of noradrenaline on RBC CO2 excretion was mimicked by the beta-adrenoceptor agonist isoproterenol, but not by the alpha-adrenoceptor agonist phenylephrine. Therefore, adrenergic inhibition of CO2 excretion is mediated by RBC beta-adrenoceptors, presumably of the beta 1 subtype. The Na+/H+ exchange inhibitor amiloride effectively blocked adrenergic stimulation of Na+/H+ exchange (as indicated from measurements of pHe and RBC pHi) and entirely prevented the inhibition of CO2 excretion. Noradrenaline significantly reduced the rate of CO2 excretion even in the presence of the Cl-/HCO3- exchange inhibitor SITS. Therefore, adrenergic inhibition of CO2 excretion is accomplished via activation of RBC Na+/H+ exchange rather than by a direct inhibition of Cl-/HCO3- exchange. The observed relationship between CO2 excretion rates and the RBC transmembrane pH difference (pHe-pHi) and the occurrence of the inhibition only at low pHe provide further evidence of the linkage with RBC Na+/H+ exchange. We suggest that adrenergic activation of RBC Na+/H+ exchange impedes CO2 excretion by causing a rise in intracellular HCO3- levels concurrent with a reduction of intracellular PCO2. The net result is a reduced gradient for HCO3- entry into the RBC in conjunction with a diminution of the outwardly directed PCO2 gradient. Thus, the rate of formation of CO2 from the dehydration of plasma HCO3- is reduced and, in turn, a portion of this CO2 is not excreted but recycled through the red blood cell.

Original languageEnglish
Pages (from-to)367-380
Number of pages14
JournalJournal of Experimental Biology
Volume157
StatePublished - May 1 1991

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Trout
Carbon Dioxide
excretion
Adrenergic Agents
trout
erythrocytes
carbon dioxide
Erythrocytes
blood
Adrenergic Receptors
norepinephrine
Norepinephrine
Oncorhynchus mykiss
epinephrine
Epinephrine
agonists
antagonists
In Vitro Techniques
inhibitor
4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Agricultural and Biological Sciences (miscellaneous)

Cite this

Adrenergic inhibition of carbon dioxide excretion by trout red blood cells in vitro is mediated by activation of Na+/H+ exchange. / Perry, S. F.; Wood, C. M.; Thomas, S.; Walsh, P. J.

In: Journal of Experimental Biology, Vol. 157, 01.05.1991, p. 367-380.

Research output: Contribution to journalArticle

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