Recently endogenous digitalis-like substances were found in the blood of various cardiovascular diseases and they have been considered one of the causes of evoking hypertension. However, the mechanism of endogenous digitalis-like
substances-induced
hypertension is not clarified yet. Therefore, the effects of Na-K pump inhibition on the contractility of vascular smooth muscle (conduit and resistant artery) were investigated, using organ bath and bioassay experiment. Aortic and carotid
arterial
rings (conduit artery) and the branches of brachial and superior mesenteric artery (resistant artery) were used to find the effect of Na-K pump inhibition.
@ES The results obtained were as followes;
@EN The magnitudes of contractions induced by norepinephrine, serotonin, or acetylcholine in all these arteries were significantly increased by the inhibition of Na-K pump. The increased contractile responses to these agonists, especially to
serotonin,
were much more prominent in resistant arteries. Nitroprusside-induced relaxations were attenuated by Na-K pump inhibition and there were no significant differences in the effects of Na-K pump inhibition on nitroprusside-induced relaxations of
these
blood vessels. Endothelium-dependent relaxation was suppressed by the inhibition of Na-K pump, especially by the administration of ouabain, and this inhibitory effect was much more prominent in the branches of superior mesenteric artery, compared
with
other arteries. In the branches of superior mesenteric arteries, endothelium-dependent relaxation was completely blocked by ouabain. The release of EDRF was partially suppressed by Na-K pump inhibition.
From the above results, it is suggested that the hypertension due to the increase in vascular resistance can be evoked y the inhibition of Na-K pump and endogenous digitalis-like substances induce hypertension through this mechanism.
(Korean J Thorac Cardiovasc Sung 1995;28:
|