Accumulation of Potassium and Calcium in Rat Myocardium Exposed to α‐1‐Adrenoceptor Stimulation
- 1 April 1992
- journal article
- Published by Wiley in Basic & Clinical Pharmacology & Toxicology
- Vol. 70 (4) , 303-307
- https://doi.org/10.1111/j.1600-0773.1992.tb00477.x
Abstract
Net fluxes of potassium, calcium, sodium and chloride were examined in isolated perfused rat hearts during α‐1‐adrenoceptor stimulation. The ion measurements were performed in the non‐recirculating perfusate. Hearts were exposed to α‐1‐adrenoceptor stimulation (phenylephrine 5×10–5mol/1 in the presence of the β‐blocker timolol 10–6mol/1). During α‐1‐adrenoceptor stimulation perfusate potassium fell relatively rapidly by about 0.10 mmol/1 after approximately 100 sec. followed by a slower rise. About 180 sec. after onset of α‐1‐adrenoceptor stimulation, the potassium level was about 0.06 mmol/1 below the control concentration level. This reduction was eliminated by the α‐1‐adrenoceptor blocker prazosin (10–7mol/1). The effects on net calcium fluxes were measured at two different calcium concentrations. For both concentrations we found a small but statistically significant reduction of the calcium concentration in the perfusate after α‐1‐adrenoceptor stimulation. Neither sodium nor chloride perfusate concentrations showed statistical significant changes compared to control values. The present observations revealed the existence of α‐1‐adrenoceptor regulated mechanisms related to a net uptake of both potassium and calcium in rat heart.Keywords
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