Experimental studies on cortisol-induced hypertension in humans.
Studies in humans have shown that cortisol administration (200 mg/day) increases cardiac output, renal vascular resistance, glomerular filtration rate, plasma volume, extracellular fluid volume, exchangeable sodium, plasma glucose, insulin, renin substrate and atrial natriuretic peptide concentrations as well as urinary kallikrein excretion. Cortisol treatment decreases renin and angiotensin II concentrations while catecholamines and vasopressin are decreased or unchanged. We have clear evidence from a number of studies that cortisol-induced hypertension is modulated by, but not dependent on, exogenous sodium. The increase in cardiac output normally seen with cortisol administration is not essential for the blood pressure rise. The role of the increase in renal vascular resistance in the genesis of the hypertension is unclear. Studies using measurements of noradrenaline spillover and assessment of reflex function have not shown any increase in sympathetic nervous system activity but changes in vascular responsiveness, particularly to phenylnephrine and noradrenaline are marked. Cortisol is known to have a variety of effects on brain, heart, kidneys, blood vessels and body fluid volumes. To what extent the observed changes are epiphenomena, amplifiers or modulators, or are causal is unclear. Cortisol hypertension may reflect a complex interplay of these factors varying with the steroid concentrations achieved, underlying genetic factors and the particular experimental circumstances.
D005110:Extracellular Space / Q000378:metabolism; D006439:Hemodynamics; D006728:Hormones / Q000096:biosynthesis; D006801:Humans; D006854:Hydrocortisone / Q000009:adverse effects*; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology; D012964:Sodium / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014666:Vasomotor System / Q000503:physiopathology
D006728:Hormones; D012964:Sodium; D006854:Hydrocortisone