RESUMEN
BACKGROUND:Potassium channel is the main ion channel to regulate vascular smooth muscle contraction and relaxation, and closely related with vascular tone. However, the reports about the mechanism of potassium channels in the body’s aging process are rare. OBJECTIVE:To investigate the effects of aging on the arterial ultrastructure and smooth muscle potassium channel reaction, and then to explore the possible mechanisms. METHODS:Sixteen healthy male Wistar rats were col ected, 19-month-old rats were assigned to the old group (n=8), 2-month-old rats were used as young group (n=8). The thoracic arteries were isolated and cut into rings to conduct contractility measurement in six rats of each group. The thoracic arteries were stimulated with specific calcium-activated potassium channel blocker tetraethylammonium, specific voltage-dependent potassium channel blocker 4-aminopyridine, specific ATP-sensitive potassium channel blocker glibenclamide, and specific inward rectifier potassium channel blocker BaCl 2 ultrastructure changes under electron microscope. , and then the arterial contractile response to the blockers were observed. The thoracic arteries of the remaining two rats in each group were taken to observe the arterial RESULTS AND CONCLUSION:Compared with the young group, the ultrastructures of the thoracic aortic endothelial cells and smooth muscle cells were changed in the old group;KCI induced the maximum thoracic aortic contractile tension, and then recovered to the baseline tension, and the recovery time in the old group was significantly longer than that in the young group;al the four kinds of blockers could increase vascular tone, and the tetraethylammonium and 4-aminopyridine induced thoracic aortic contractile response in the old group was significantly lower than that in the young group;there was no significant difference in vasoconstriction induced by glibenclamide and BaCl 2 . Aging can induce arterial ultrastructure changes and declination of vasodilatation capacity, which may partly due to the decreasing of the potassium channels function in smooth muscle cells, especial y the calcium-activated potassium channel and inward rectifier potassium channel.