Showing papers by "Laura Soldati published in 1997"
TL;DR: The hypothesis that erythrocyte Ca2+ influx is mediated by a carrier similar to the slow Ca2-chelator channels and is dependent on membrane depolarization is supported.
28 citations
7 citations
TL;DR: It is suggested that a genetic alteration of proximal tubular function could cause multiple reabsorption defects in the Proband or renal phosphate leakage in the proband's relatives.
4 citations
TL;DR: The data seem to suggest that increased protein degradation by calpain may prevent the development of LVH in hypertensive patients, independent of the duration and severity of hypertension.
Abstract: 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, R 2 = 7.9%). This relation was still present considering only untreated hypertensives (P = 0.008; R 2 = 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.
3 citations