Membrane Potential Of Endothelial Cells Research Articles

Endothelial and smooth muscle cells hyperpolarized by bradykinin are not dye coupled

The membrane potential of endothelial and neighboring (0.1 mm) smooth muscle cells of pig coronary arteries were simultaneously recorded with two microelectrodes. The membrane potential of endothelial cells was -40 +/- 4 mV (n = 9). In these cells bradykinin (250 nM), an endothelium-dependent vasodilator, evoked a transient hyperpolarization (14 +/- 2 mV, n = 9) resembling those already observed in smooth muscles. The similarity between the electrical signal of pre- and postmyoendothelial junctions suggested an electrical coupling between endothelial and smooth muscle cells. However, the injection of the fluorescent dye Lucifer yellow in the recorded cell proved that the cell was endothelial, and in addition, the injection demonstrated the absence of dye coupling between endothelial and smooth muscle cells. Moreover the injection of electrical pulses (0.05-3.5 nA) in the endothelial cell never evoked any electrical response in the smooth muscle. By contrast, the smooth muscle cells were electrically coupled-together. These results do not support the idea that the endothelial cell hyperpolarization caused by bradykinin is transmitted to smooth muscle cells by electrotonic spreading.

Effects of changes in extra‐ and intracellular K+ on the endothelial production of prostacyclin

1. Changes in the KCl concentration of the incubation medium, from 0 to 80 mM, had no effect on the basal or ATP-stimulated release of prostacyclin (PGI2) from bovine aortic endothelial cells. 2. The monovalent cation ionophores, valinomycin and nigericin (5 microM), enhanced the release of PGI2 from endothelial cells stimulated by ATP or bradykinin. 3. The action of nigericin, unlike that of valinomycin, was time-dependent, abolished in a high-KCl medium and associated with an increased efflux of 86Rb and a time-dependent depletion of intracellular K+. 4. Ouabain (1-100 microM) also enhanced the release of PGI2 in response to ATP and induced a significant depletion of intracellular K+ in bovine aortic endothelial cells. 5. In conclusion, modifications of the endothelial cell membrane potential, resulting from changes in the extracellular K+ concentration, do not modulate the basal or ATP-stimulated production of PGI2. An acute depletion of intracellular K+ by nigericin or ouabain enhances the production of PGI2 in aortic endothelial cells stimulated by ATP or bradykinin.

Substance P and Bradykinin Hyperpolarize Pig Coronary Artery Endothelial Cells in Primary Culture

Substance P (SP) and bradykinin (BK) relax and hyperpolarize smooth muscles of pig coronary arteries in an endothelium-dependent manner. We investigated the effect of both peptides on the membrane potential of endothelial cells in culture. The membrane potential of pig coronary artery endothelial cells in primary culture was -44 mV. SP and BK hyperpolarized it transiently by 23 mV. These hyperpolarizations were dependent on the potassium gradient across the cellular membrane. They had similar time courses as the SP and BK endothelium-dependent hyperpolarizations already observed in smooth muscles.