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Plasma cortisol and corticosteroid-binding globulin in essential hypertension
W Nowaczynski1, G E Wilkins, T Murakami
1Steroid Research Laboratory, St. Paul's Hospital, Vancouver, B.C., Canada.
Clinical Physiology and Biochemistry
|January 1, 1988
Summary
Essential hypertension (EH) patients and their relatives show decreased plasma cortisol and reduced cortisol-binding globulin (CBG) binding capacity. These steroid metabolism alterations may contribute to hypertension development.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Genetics
Background:
- Essential hypertension (EH) is a complex cardiovascular condition with multifactorial origins.
- Cortisol-binding globulin (CBG) plays a crucial role in regulating cortisol bioavailability.
- Alterations in steroid hormone metabolism and binding proteins are implicated in hypertension pathogenesis.
Purpose of the Study:
- To investigate plasma cortisol levels, CBG-binding capacity, and aldosterone levels in patients with essential hypertension (EH) and their normotensive (NR) and hypertensive (HR) relatives.
- To explore the correlation between these hormonal parameters and mean arterial pressure (MAP).
- To elucidate potential steroid metabolism abnormalities contributing to EH.
Main Methods:
- Cross-sectional study measuring plasma cortisol, CBG-binding capacity, aldosterone, and aldosterone-binding globulin (ABG) binding capacity.
- Participants included controls, EH patients, and their first-degree relatives (NR and HR).
- Statistical analysis included comparisons of means and correlation analyses between hormonal levels and MAP.
Main Results:
- EH patients and HR relatives exhibited significantly lower plasma cortisol and CBG-binding capacity compared to controls.
- Plasma cortisol in NR did not differ from controls, but their CBG-binding capacity was also reduced.
- Elevated plasma aldosterone was observed in EH patients, with a positive correlation between MAP and ABG-binding capacity across all subjects.
Conclusions:
- Reduced plasma cortisol and decreased CBG-binding capacity in EH patients and relatives suggest altered steroid metabolism.
- These findings may indicate a relative deficiency in adrenal 17 alpha- and 11 beta-hydroxylation.
- Hypertension in some EH patients could stem from cortisol's ineffectiveness in suppressing elevated ACTH levels, leading to increased ACTH-sensitive steroids.