ISSN:
1432-1912
Keywords:
Pinacidil
;
K+-channels
;
Membrane potential
;
Ion flux
;
Blood vessels
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary In rat aorta and rat portal vein, (−)- and (+)-pinacidil each produced a concentration-dependent inhibition of tension development. Although the (−) isomer was the more potent, concentration effect curves for each isomer were steep with similar slopes. In rat portal vein, tetraethylammonium and procaine antagonised the relaxant effect of (±)-pinacidil, whereas 3,4-diamino-pyridine was without effect. Intracellular microelectrode recording in rat portal vein showed that low concentrations of (±)-pinacidil reduced the duration of multispike electrical complexes. In both rat aorta and rat portal vein, higher concentrations of (±)-pinacidil hyperpolarised the membrane towards the potassium equilibrium potential. (±)-Pinacidil increased 86Rb efflux from rat aorta and rat portal vein in a concentration dependent manner. In a separate study, (±)-pinacidil increased 42K efflux from rat portal vein. (±)-Pinacidil had no effect on cyclic GMP or cyclic AMP levels in rat aorta. It is concluded that pinacidil opens 86Rb-permeable potassium channels in rat aorta and rat portal vein. This mechanism is independent of cyclic nucleotide changes and may be responsible for the antihypertensive effect of pinacidil.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00173406
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