|
pubmed:abstractText |
The data presented establish that in early or mild essential hypertension there is a state of inappropriate hypermineralocorticoid activity represented by the sum of aldosterone and 18-hydroxy-11-deoxycorticosterone concentrations in the plasma. This disturbance, associated with a "normal" or excessive salt intake, would produce the arteriolar cationic changes in sodium, potassium, calcium, or magnesium leading to hypersensitivity or hyperresponsiveness of the arteriolar actomyosin to normal levels of circulating norepinephrine or angiotensin. The nature of the cationic changes in the arteriolar cells responsible for the increased tonicity of the arteriolar actomyosin, which is the fundamental cause of essential hypertension, remains to be elucidated.
|
