Related Experiment Videos
Experimental studies on cortisol-induced hypertension in humans
J A Whitworth1, M A Brown, J J Kelly
1Department of Medicine, St. George Hospital, Kogarah, NSW, Australia.
Journal of Human Hypertension
|June 1, 1995
Summary
Cortisol administration in humans increases cardiac output and fluid volumes, leading to hypertension. This blood pressure rise is not solely dependent on sodium levels and involves complex vascular and hormonal interactions.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
- Renal Physiology
Background:
- Cortisol, a key stress hormone, significantly impacts multiple physiological systems.
- Previous research indicates cortisol influences blood pressure regulation through various mechanisms.
Purpose of the Study:
- To elucidate the multifaceted effects of cortisol administration on human cardiovascular and fluid balance.
- To investigate the mechanisms underlying cortisol-induced hypertension, including the roles of sodium, cardiac output, and vascular responsiveness.
Main Methods:
- Human studies involving cortisol administration (200 mg/day).
- Measurements of cardiac output, renal vascular resistance, glomerular filtration rate, and plasma/fluid volumes.
- Assessment of hormonal changes (renin, angiotensin II, catecholamines, vasopressin, insulin, ANP) and sympathetic nervous system activity.
Main Results:
- Cortisol increased cardiac output, renal vascular resistance, GFR, plasma volume, extracellular fluid volume, exchangeable sodium, glucose, insulin, renin substrate, and ANP.
- Cortisol decreased renin and angiotensin II; catecholamines and vasopressin were decreased or unchanged.
- Cortisol-induced hypertension was modulated by, but not dependent on, exogenous sodium.
- Increased cardiac output was not essential for the blood pressure rise; the role of renal vascular resistance was unclear.
- No increase in sympathetic nervous system activity was detected, but vascular responsiveness to certain agents was markedly altered.
Conclusions:
- Cortisol exerts broad physiological effects contributing to hypertension through complex interactions.
- The development of cortisol-induced hypertension involves intricate interplay between hormonal changes, fluid volume shifts, vascular responsiveness, and potentially genetic factors.