Intracellular Na+ as a genetic marker of essential hypertension.
In 1960 the pathophysiological mechanisms by which Na+ is involved in human essential hypertension were first elucidated by the finding that intracellular Na+ is elevated in red blood cells of essential hypertensives. Furthermore it was found that (1) transmembranous Na+ fluxes in red blood cells of essential hypertensives are changed in parallel with intracellular Na+ concentration, reflecting the metabolic disturbances better than the Na+ concentration measurements, (2) in normotensives with a familial disposition of essential hypertension intracellular Na+ and transmembranous Na+ fluxes are elevated, (3) uremia affects intracellular Na+ levels similarly as essential hypertension, and (4) intracellular free Na+ and free Ca++ is increased in spontaneously hypertensive rats. It can be assumed that elevated intracellular Na+ plays a causative role in essential hypertension.
D000818:Animals; D004195:Disease Models, Animal; D004912:Erythrocytes / Q000378:metabolism; D005819:Genetic Markers; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000378:metabolism*; D006978:Hypertension, Renovascular / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000097:blood / Q000378:metabolism*
D005819:Genetic Markers; D012964:Sodium; D011188:Potassium