Deviation of plasmatic aldosterone and significance of the stimulating (ACTH-cortrosyn) and inhibitory (propranolol) effects in hypertension and cardiovascular pathology.
Starting from the interference between the renin-angiotensin-aldosterone (RAA) system and cardiovascular pathology in arterial hypertension (AH) we have made a correlative study of the cardiovascular system and plasmatic aldosterone in normal and hypertensive subjects under conditions of stimulation (ACTH) and inhibition (propranolol). After administration of ACTH (one of the physiologic mediators of stress) increased values for plasmatic aldosterone were found. Negative cardiovascular effect: arrhthmia, angor, AH, cardiac asthma, under the condition of preexisting cardiovascular pathology or altered steroidogensis, were also noticed. Inhibition with propranolol does not have conclusive effects in AH with normal aldosterone. The best effect were noticed in that hypertension which implies the RAA pressor system in its pathogeny, irrespective of etiology, the reduction AT occurring in parallel with decline in plasmatic aldosterone values and total peripheral resistance (RPT). Administration of propranolol in AH with activated RAA system irrespective of etiology represents a pathogenic treatment able to prevent efficiently the major complications of AH.
D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000328:Adult; D000450:Aldosterone / Q000097:blood*; D002319:Cardiovascular System / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D011433:Propranolol / Q000494:pharmacology* / Q000627:therapeutic use; D013256:Steroids / Q000096:biosynthesis
D013256:Steroids; D000450:Aldosterone; D000324:Adrenocorticotropic Hormone; D011433:Propranolol