β2‐ADRENOCEPTORS MEDIATE THE STIMULATING EFFECT OF ADRENALINE ON ACTIVE ELECTROGENIC NA‐K‐TRANSPORT IN RAT SOLEUS MUSCLE
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The relative role of beta 1- and beta 2-adrenoceptors in mediating the stimulating effect of adrenaline on active electrogenic Na-K-transport has been assessed in experiments on rat soleus muscles in vitro and in vivo. 2 In the rat isolated soleus muscle, adrenaline (10(-6) M) increases the resting membrane potential (EM) by 5.8 mV and stimulates 22Na-efflux and ouabain-suppressible 42K-uptake by 91 and 94%, respectively. 3 All of these effects are completely blocked by propranolol (10(-5) M), whereas the beta 1-selective adrenoceptor antagonist, metoprolol, was found to be at least 50 times less potent. 4 The beta 2-adrenoceptor agonist, salbutamol, was at least 100 times as potent as H133/22 (a beta 1-selective agonist) in stimulating 22Na-efflux and 42K-influx. 5 In experiments performed under pentobarbitone anaesthesia, the intravenous injection of adrenaline (5 microgram) or salbutamol (0.5 to 50 microgram) led to a rapid and marked increase in the EM of the exposed soleus muscle. This hyperpolarizing effect could not be accounted for by the concomitant, relatively modest change in extracellular K.
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Adrenaline infused into animals and, in high dose, to man causes a decrease in serum potassium.
“Adrenaline infused into animals7 I I and, in high dose, to man12 causes a decrease in serum potassium.”
From Effect of intravenous adrenaline on electrocardiogram, blood pressure, and serum potassium. (1983) · cites this paper as [11]
The Introduction (page unavailable) states that catecholamines induce hypokalaemia in the intact organism, supporting the general potassium-lowering effect attributed to adrenaline. The Results report intravenous adrenaline in rats but measure serum potassium after salbutamol, not adrenaline; our copy does not establish the claim about high-dose adrenaline in humans. (LLM, conf=0.83)
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- Authors
- CLAUSEN, T., & FLATMAN, J. A.
- Affiliations
- Aarhus University (DK)
- ORCID
- CLAUSEN, T.
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 1980-04
- Volume
- 68
- Issue
- 4
- Pages
- 749-755
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC2044229
- OpenAlex
- W2031109036
- Cited by
- 246
- References
- 19
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2022: 3 · 2021: 5 · 2020: 3 · 2019: 3 · 2018: 1 · 2017: 4 · 2016: 3 · 2015: 4 · 2014: 3 · 2013: 3 · 2012: 2
- FWCI
- 5.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- beta2-adrenergic receptor, beta1-adrenergic receptor, epinephrine, salbutamol, Na+/K+-ATPase, soleus muscle, resting membrane potential, propranolol, metoprolol, potassium uptake, sodium efflux, skeletal muscle
- MeSH terms
- Albuterol, Animals, Biological Transport, Active, Epinephrine, Female, Male, Membrane Potentials, Muscles, Potassium, Receptors, Adrenergic, Receptors, Adrenergic, beta, Sodium, Time Factors, Rats, In Vitro Techniques
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