Key result
Superfusion with 2 microM adenosine elicited a transient (15 ± 6 mV) or sustained (11 ± 3 mV) hyperpolarization in cultured guinea pig coronary endothelial cells.
Adenosine induces hyperpolarization in guinea pig coronary endothelial cells, suggesting a mechanism for coronary vasodilation via myoendothelial gap junctions.
May inform preclinical mechanisms of coronary vasoregulation; leaves open translation to human physiology and clinical relevance.
Electrophysiological experiments on cultured monolayers of guinea pig coronary endothelial cells were performed to substantiate the hypothesis that variation of the endothelial membrane potential may be a functionally important mechanism that contributes to the regulation of coronary blood flow. The endothelial cells were loaded with sodium by superfusion with K(+)-free solution at 37 degrees C for 5-30 min. Readmission of external K+ produced a transient hyperpolarization of up to 85 mV, which was due to stimulation of the electrogenic pump current. In most but not all of the monolayers, superfusion with 2 microM adenosine elicited a transient or a sustained hyperpolarization. The transient hyperpolarization had an amplitude of 15 +/- 6 mV. The sustained hyperpolarization had an amplitude of 11 +/- 3 mV. Our results are in line with the hypothesis that the hyperpolarization of the endothelium induced by release of adenosine into the perivascular space of the capillaries may be conducted electronically to the terminal arterioles and may cause vasodilation via current flow through myoendothelial gap junctions.
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Seiss-Geuder et al. (1992) studied this question. Adenosine was evaluated on Hyperpolarization. Superfusion with 2 microM adenosine elicited a transient (15 ± 6 mV) or sustained (11 ± 3 mV) hyperpolarization in cultured guinea pig coronary endothelial cells.
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