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PAI-1 in human hypertension: relation to hypertensive groups
Nadarajah Srikumar1, Nancy J Brown, Paul N Hopkins
1Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Insights
Dietary salt restriction increased plasminogen activator inhibitor type-1 (PAI-1) levels in hypertensive patients. Aldosterone (ALDO) showed a significant correlation with PAI-1, suggesting its role in PAI-1 variability.
Area of Science:
- Cardiovascular Medicine
- Endocrinology
- Metabolic Syndrome
Background:
- The renin-angiotensin system and insulin resistance (IR) are known regulators of plasminogen activator inhibitor type-1 (PAI-1).
- Their specific roles in hypertensive individuals remain unclear.
Purpose of the Study:
- To investigate the impact of dietary salt restriction on PAI-1 levels in hypertensive subjects.
- To explore the correlations between PAI-1, plasma renin activity (PRA), insulin resistance (IR), and aldosterone (ALDO).
Main Methods:
- 239 hypertensive subjects underwent dietary salt restriction (200 and 10 mmol/day).
- PAI-1 and PRA levels were measured. Fasting insulin, glucose, and ALDO were assessed on low-salt diet.
- Subjects were categorized into low renin, nonmodulators, and modulators groups.
Main Results:
- Sodium restriction significantly increased PAI-1 levels (P = .009).
- PAI-1 positively correlated with PRA, IR, triglycerides, and ALDO.
- Modulators group exhibited significantly higher PAI-1 levels compared to other groups.
Conclusions:
- PRA, IR, and ALDO are correlated with PAI-1 levels in hypertensive patients.
- Aldosterone may significantly contribute to individual variations in PAI-1 levels among hypertensive subjects.
Background:
Although the renin-angiotensin system and insulin resistance (IR) have been identified as major regulators of plasminogen activator inhibitor type-1 (PAI-1), their roles in hypertensive subjects is not clearly defined.
Methods:
We examined the effect of dietary salt restriction on PAI-1 levels in 239 hypertensive subjects from three centers. Subjects were placed on a 200 and 10 mmol/day sodium diets for 1-week periods. Plasma renin activity (PRA) and PAI-1 levels were measured on the last day of both diets and fasting insulin, glucose, and aldosterone (ALDO) levels, only on the low salt diet.
Results:
Sodium restriction increased PAI-1 levels from 32.1 +/- 2.5 ng/mL to 39.8 +/- 3.2 ng/mL (P = .009). There was a strong positive correlation between PAI-1 levels and PRA (r = 0.228, P = .0004), IR (r = 0.222, P = .001), triglycerides (r = 0.275, P < .001), and ALDO (P = .018 for linear trend). The patients were divided into low renin (low IR and ALDO levels), nonmodulators (normal PRA, high IR, and low ALDO levels), and modulators (normal PRA, intermediate IR, and normal ALDO levels) groups to assess the relative contribution of each factor to PAI-1 levels. Modulators had significantly (P = .019) higher PAI-1 levels compared to the low renin and nonmodulators who had similar PAI-1 levels.
Conclusions:
Plasma renin activity, IR, and ALDO all correlate with PAI-1 levels in the hypertensive subjects. However, the data suggest that ALDO may be an important factor contributing to the variability of PAI-1 levels in individual hypertensive subjects.