Knowledge of the hormonal peculiarities of essential arterial hypertension may direct therapy and prevent errors.
The endocrine system becomes involved in the physiopathologic mechanisms of essential arterial hypertension (EAH) by the interference of hormones with the pressor and depressor substances. A "depressor" pharmacodynamic model with beta-blockers based on the variations of hormone-dependent data offers a series of characteristics for assessing the vasoconstrictive and volemic components, evolution (accelerated for instance) and treatment. Hormone data are also useful for avoiding errors and for increasing the efficiency and control of the therapy. It is not uncommon for EAH to become endocrine-dependent, for instance: increase in aldosterone secretion by activation of the renin-angiotensin (RA) system or of the hypophysis- corticoadrenal system and the adreno-sympathetic system, transforms the relatively "benign" evolution of EAH into an "accelerated" one. The incidence of hyperreactive corticoadrenal (with or without altered steroidogenesis), corticoadrenal hyperplasia or adenoma, is in reality higher than commonly diagnosed.
D000319:Adrenergic beta-Antagonists; D000308:Adrenocortical Hyperfunction / Q000150:complications; D000328:Adult; D000450:Aldosterone / Q000097:blood; D002395:Catecholamines / Q000652:urine; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006973:Hypertension / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000097:blood
D000319:Adrenergic beta-Antagonists; D002395:Catecholamines; D000450:Aldosterone; D012083:Renin; D006854:Hydrocortisone