Alteration of cellular calcium metabolism as primary cause of hypertension.
In the pathogenesis of hypertension, the importance of intracellular calcium is increasing. Clinical and experimental studies of essential hypertension indicate a pathological increase of intracellular Ca2+ in this disease. In the past, changes in cellular Na+ and its transport mechanisms were considered the triggering factors and Na+-Ca2+ exchange was attributed a decisive influence on intracellular homeostasis. Recently, a reduced Ca2+-binding capacity of the cellular membrane was observed in hypertension, which could have been due to a defect of the Ca2+-ATPase or its control. It is therefore necessary to establish the hypothesis that changes in the cellular Ca2+ metabolism associated with an increase in the intracellular Ca2+ concentration may be the primary cause of hypertension. Disorders of Na+ transport can also be traced to the increase in intracellular Ca2+ and were thus a consequence but not the cause of the increased intracellular Ca2+ concentration.
Sprenger
K B
KB
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D006801:Humans; D006973:Hypertension / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism; D009638:Norepinephrine / Q000494:pharmacology; D011494:Protein Kinases / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism
D002121:Calcium Channel Blockers; D000255:Adenosine Triphosphate; D012964:Sodium; D011494:Protein Kinases; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D002118:Calcium; D009638:Norepinephrine