The sodium-potassium pump in volume expanded hypertension.
Decreased arterial Na+-K+ pump and cardiac Na+, K-+ATPase activities have now been demonstrated in several types of experimental volume expanded hypertension. The changes are not secondary to elevated pressure since they also occur in veins and right ventricle where the pressure is not elevated. Decreased arterial Na+-K+ pump activity can be reproduced by acute volume expansion of the normal rat and plasma extracts from this rat suppress pump activity when applied to arteries from another rat. Suppression of Na+-K+ pump activity in arteries, veins and heart, with ouabain for example, leads to increased contractile activity. Thus the volume expansion, reduced pump activity, and hypertension appear to be causally related through an ouabain-like humoral agent. Certain other evidence suggests that the pump defect extends to the sympathetic nerve endings, thereby reducing the efficiency of neural compensatory mechanisms.
D000818:Animals; D001794:Blood Pressure; D001810:Blood Volume; D002319:Cardiovascular System / Q000378:metabolism*; D003900:Desoxycorticosterone; D004285:Dogs; D006801:Humans; D006973:Hypertension / Q000139:chemically induced / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D006977:Hypertension, Renal / Q000378:metabolism; D007676:Kidney Failure, Chronic / Q000150:complications; D009392:Nephrectomy; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D012965:Sodium Chloride; D013564:Sympathetic Nervous System / Q000503:physiopathology
D003900:Desoxycorticosterone; D012965:Sodium Chloride; D012964:Sodium; D011188:Potassium