Low renin hypertension.
Low renin hypertension probably does not represent a clinical entity. In many patients with low renin hypertension blood pressure is normalized by treatment with diuretics only; in these patients a (genetic?) sensitivity to salt might play a predominant role in the pathogenesis of hypertension and renin suppression. In another group of patients renin suppression appears to be secondary to the hypertensive process. This is indicated by the observation that prevalence of low renin hypertension increases with age and that it is more frequent in advanced stages of hypertension. Also a diminished sympathetic tone might play a part in the renin unresponsiveness. Finally, although no positive evidence was found, the possibility cannot be excluded that, at least in some cases, a mineralocorticoid other than aldosterone is involved. Neither in normotensive subjects nor in hypertensive patients, both with normal and with low plasma renin was a correlation between plasma renin concentration and plasma aldosterone concentration following stimulation by upright posture found. More detailed studies will be necessary to clarify the relationship between the renin-angiotensin system and aldosterone secretion during upright posture, in particular in patients with low renin hypertension.
D000302:Adrenal Cortex / Q000503:physiopathology; D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D008664:Metal Metabolism, Inborn Errors / Q000150:complications; D011187:Posture; D012083:Renin / Q000097:blood* / Q000172:deficiency / Q000378:metabolism; D012965:Sodium Chloride / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology
D012965:Sodium Chloride; D000450:Aldosterone; D012083:Renin; D006854:Hydrocortisone