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Erythrocyte calpain activity and left ventricular mass in essential hypertension
P Stella1, L Soldati, D Ciurlino
1Milan University, S. Raffaele Hospital, Italy.
Insights
Calpain activity in erythrocytes may prevent left ventricular hypertrophy (LVH) in essential hypertension. This inverse relationship suggests a protective role for calpain in hypertensive heart disease, independent of hypertension severity.
Area of Science:
- Cardiovascular Physiology
- Molecular Biology
- Hypertension Research
Background:
- Calpains are cytoplasmic proteases found in eukaryotic cells.
- Previous studies showed low calpain activity in rat hearts with hypertension-induced hypertrophy.
- The role of calpain in human hypertensive cardiac hypertrophy remained unclear.
Purpose of the Study:
- To investigate the role of calpain activity in the development of left ventricular hypertrophy (LVH) in human essential hypertension.
- To explore the relationship between erythrocyte calpain activity and left ventricular mass index (LVMI) in hypertensive patients.
Main Methods:
- Studied 115 patients with essential hypertension (72 untreated, 43 treated).
- Measured calpain I activity in erythrocytes.
- Assessed LVH using left ventricular mass index (LVMI) via M-mode echocardiography.
Main Results:
- An inverse relationship was observed between LVMI and erythrocyte calpain activity in all hypertensive patients (P = 0.0023).
- This inverse relation persisted in untreated hypertensives (P = 0.008) but was absent in treated patients.
- In untreated hypertensives, stepwise regression identified calpain activity and mean arterial pressure as significant predictors of LVMI.
Conclusions:
- Erythrocyte calpain activity may serve as a biomarker for calpain levels in cardiomyocytes.
- Increased calpain activity might protect against LVH development in hypertensive patients.
- This potential protective effect of calpain appears independent of hypertension duration and severity.
Background:
Calpains are cytoplasmic proteases widely distributed among eucaryotic cells. Low levels of calpain activity were found in hypertrophic hearts from hypertensive rats, but its role in hypertrophic hearts from human hypertensives is unknown. Therefore, calpain activity was investigated in erythrocytes from essential hypertensive patients in relation to their left ventricular mass.
Objective:
To study the role of calpain activity in the development of left ventricular hypertrophy (LVH) in human essential hypertension.
Methods:
A total of 115 hypertensives (72 untreated and 43 with treatment interrupted for at least 4 months) were included in the study. Calpain I activity was measured in human erythrocytes and LVH was measured as left ventricular mass index (LVMI) by M-mode echocardiography.
Results:
Values are given as mean+/-SEM. The hypertensives (97 men and 18 women) were 43.5+/-0.9 years old with mild to moderate levels of hypertension (systolic/diastolic blood pressure of 147.9+/-1.4/98.7+/-0.9 mmHg) and relatively recent LVH onset (3.5+/-0.5 years). An inverse relation between LVMI and erythrocytic calpain activity was present in all (P = 0.0023, R2 = 7.9%). This relation was still present considering only untreated hypertensives (P = 0.008; R2 = 9.7%), but was lost in the 43 previously treated hypertensives. Moreover, in the untreated hypertensives, after excluding the possible confounding effects of sex, age, body mass index, blood pressure and duration of hypertension, a stepwise regression showed that only two variables remained significantly related to LVMI: calpain (F = 6.23) and mean arterial pressure (F = 4.689). No relations were found between LVMI and calpastatin activity either in the whole population, or in treated or untreated hypertensives.
Conclusions:
If we assume that the level of erythrocyte calpain activity mirrors the level in cardiomyocytes, these data seem to suggest that increased protein degradation by calpain may prevent the development of LVH in hypertensive patients. This effect is independent of the duration and severity of hypertension.