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Hypertension and the kidney
1Department of Medicine, University of New South Wales, Australia.
Insights
Research explores hypertension, focusing on vascular lesions and renal parenchymal disease. Studies suggest impaired cortisol-cortisone shuttle and 11-beta-HSD activity contribute to steroid-induced hypertension.
Area of Science:
- Nephrology
- Endocrinology
- Cardiovascular Research
Background:
- Priscilla Kincaid-Smith's work on hypertension pathogenesis, particularly vascular lesions.
- Investigating the role of the cortisol-cortisone shuttle and 11-beta-hydroxy-steroid dehydrogenase in renal parenchymal disease hypertension.
- Defining renal functional consequences of steroid-induced hypertension.
Discussion:
- Glucocorticoid-induced hypertension is independent of volume/sodium status but modulated by dietary sodium.
- Normal pregnancy involves adaptation to sodium extremes, unlike pre-eclampsia.
- Pre-eclampsia is characterized by sodium retention and enhanced capillary permeability.
Key Insights:
- Impaired cortisol-cortisone shuttle and reduced 11-beta-HSD activity in renal hypertension.
- Steroid-induced hypertension mechanisms elucidated, independent of volume shifts.
- Pre-eclampsia pathophysiology involves abnormal aldosterone:renin ratio, dopaminergic pathways, natriuretic peptides, and prostacyclin:thromboxane balance.
Outlook:
- Further research into the cortisol-cortisone shuttle's role in hypertension.
- Exploring therapeutic targets for steroid-induced and pre-eclampsia-related hypertension.
- Investigating the interplay of hormonal and vascular factors in hypertensive disorders.
Abstract:
From our perspective, Priscilla Kincaid-Smith's major achievement in the field of hypertension relates to the pathogenesis of vascular lesions. Our own studies of the hypertension of renal parenchymal disease have suggested a role for impairment of the cortisol-cortisone shuttle and decreased activity of the enzyme complex 11-beta-hydroxy-steroid dehydrogenase. We have defined the renal functional consequences of steroid-induced hypertension and shown that the rise in blood pressure produced by steroids with predominant glucocorticoid activity is not dependent on volume shifts or sodium status, although the magnitude of the rise is modulated by dietary sodium content. We have shown that normal pregnant women adapt readily to extremes of sodium intake while women with pre-eclampsia retain sodium, and have shown enhanced capillary permeability. Recent studies have defined an abnormal aldosterone:renin ratio, dopaminergic inhibition of aldosterone, elevations of plasma atrial natriuretic peptide and reduced urinary prostacyclin:thromboxane ratios in women with pre-eclampsia.