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Biomedical subjects

A De la Sierra

Publications and source records attributed to A De la Sierra.

11 recordsLinked to original sources
PubMed1997

Salt sensitivity and left ventricular hypertrophy.

Essential hypertensive patients with left ventricular hypertrophy (LVH) increase their mortality rates due to all cardiovascular diseases from 3 to 10 times more than hypertensives without signs of cardiac hypertrophy. LVH modifies the equilibrium between the oxygen supply and demand by the myocardium. The coronary reserve is appreciably reduced in hypertensives with LVH even in the absence of any stenosis of coronary arteries. Thus, in patients with normal coronary angiogram, a predisposition toward myocardial ischemia already exists. This process has been associated with the increased incidence of ventricular arrhythmias in essential hypertensives with LVH, what could be linked to the increasing risk of sudden death in these patients. In addition to hemodynamic factors (pressure and volume overload) several non-hemodynamic factors have been involved in the pathogenesis of LVH in hypertension. LVH would develop in subjects with a particular genetic substrate by the overlap of high blood pressure values and several factors linked to the adrenergic system, the renin-angiotensin-aldosterone system, other vasoactive substances, and growth factors. It has been previously reported that NaCl ingestion is a powerful determinant of left ventricular hypertrophy in patients with essential hypertension. Furthermore, a relationship between left ventricular mass and abnormalities in intracellular Na+ or transmembrane Na+ transport has been observed in several studies. Salt-sensitive hypertensive subjects seem to exhibit an increased risk in terms of cardiovascular morbidity. We and others have observed a higher left ventricular mass, an increased albumin excretion rate and a worse lipid profile in salt-sensitive compared with salt-resistant patients. The increase in LVMI in salt-sensitive patients is mainly due to the increase in septal and posterior wall thickness, with normal diastolic diameter, suggesting that myocardial growth in these patients is not volume-dependent. The mechanism of this structural cardiac adaptation is not completely understood. Nevertheless, it is known that salt-sensitive and salt-resistant hypertensive patients differ in some adaptive responses to changes in dietary salt intake. Among them, the renin-aldosterone axis, the sympathetic nervous system and the intracellular ion composition could play a role in the development of myocardial growth. In conclusion, salt-sensitive hypertensive patients exhibited an increased LVMI and a worse lipid profile, compared with salt-resistant hypertensives, even at the same level of blood pressure. These characteristics may confer to salt-sensitive patients an increased risk in terms of cardiovascular morbidity and mortality.

Adult↗
PubMed1996

A multicenter, parallel comparative study of the antihypertensive efficacy of once-daily lisinopril vs enalapril with 24-h ambulatory blood pressure monitoring in essential hypertension.

The aim of the study was to compare the antihypertensive efficacy of once-daily lisinopril vs enalapril both during normal daily activity and sleep, in mild-to-moderate essential hypertension. After a 4-week wash-out period, 34 patients (17 M, 17 F) aged 22 to 67 years were randomized in a multicenter, open, parallel fashion: 17 received lisinopril (10-20 mg) and 17 enalapril (10-20 mg) for a 12-week period. Twenty-four hour ambulatory blood pressure monitoring (ABPM) was performed using an oscillometric non-invasive automated device at both the end of the 4-week drug-free baseline period and during the last week of treatment. With no differences in initial blood pressure (BP) between groups, both drugs significantly reduced office and ABPM values. Lisinopril tended to reduce BP in a greater extension than enalapril, but only the reduction of office systolic BP (SBP) (p = 0.0062), 24-h SBP load (P = 0.0182) and night time SBP load (P = 0.0316) reached statistical significance. We conclude that, in spite of a more prominent reduction of SBP by lisinopril, both drugs have a similar efficacy in reducing BP, assessed by both office and ABPM measurements.

Adult↗
PubMed1993

Comparative evaluation of the antihypertensive efficacy of once-daily amlodipine versus nitrendipine with 24-hour ambulatory blood pressure monitoring in essential hypertension.

We compared the antihypertensive efficacy of once-daily amlodipine (AM) versus nitrendipine (NTR) by 24-h ambulatory blood pressure monitoring (24-h ABPM) in 32 patients with mild to moderate essential hypertension (EH). After a 2-week single-blind, placebo run-in period, patients were randomized in a double-blind, parallel fashion: 14 received AM 5 mg and 18 NTR 10 mg. After 2 weeks, dose was adjusted if necessary (AM 10 mg or NTR 20 mg) and continued for another 6-week period. At the end of the placebo period and during the last week of treatment, patients underwent 24-h ABPM. Initial office BP mean values were similar in both groups (169.8 +/- 14/102.5 +/- 6 vs. 167.1 +/- 14/98.7 +/- 5 mm Hg, respectively, p = NS). A comparable decrease in office mean values of systolic BP (SBP, -22.3 +/- 13 vs. -19.1 +/- 16 mm Hg) and diastolic BP (DBP, -12.0 +/- 5 vs. -8.1 +/- 8 mm Hg) was observed. Nevertheless, 24-h ABPM mean values differed significantly between patients treated with AM or NTR with regard to 24-h SBP (120.0 +/- 10 vs. 132.5 +/- 1 mm Hg, p = 0.01). Moreover, the average decrease in 24-h SBP (-19.3 +/- 6 vs. -5.2 +/- 11 mm Hg, p = 0.0036) and 24-h DBP (-10.7 +/- 4 vs. -3.7 +/- 6 mm Hg, p = 0.0047) was higher in the AM group, with no changes in 24-h heart rate (HR). At equivalent once-daily dosage, AM was more effective than NTR in decreasing BP assessed by 24-h ABPM.

Adult↗
PubMed1992

Chronic alcohol intake induces reversible disturbances on cellular Na+ metabolism in humans: its relationship with changes in blood pressure.

The effect of chronic alcohol consumption on Na(+)-K+ ATPase, Na(+)-Li+ countertransport, outward Na(+)-K(+)-Cl- cotransport system and the Na+ leak was investigated in red blood cells from 18 normotensive subjects with a daily alcohol intake of more than 150 g. The study was repeated after 3 months of alcohol withdrawal, and results were compared with a group of 20 healthy normotensive teetotalers. Maximal efflux rate (Vmax) and apparent dissociation constant for internal Na+ (KNa) of the Na(+)-K+ pump and the Na(+)-Li+ countertransport were significantly higher in alcohol consumers. A positive correlation between daily alcohol intake and Vmax of both transport systems (p less than 0.05) was observed. These values significantly decreased after alcohol withdrawal. A simultaneous stimulation of the Na(+)-K(+)-Cl- cotransport system after alcohol withdrawal was also observed. Blood pressure values were higher in alcoholics (133.7/82.3) than in abstainers (121.4/75 mmHg) and significantly decreased (128.5/76.9 mmHg) after withdrawal. A positive correlation between the stimulation of the Na(+)-K(+)-Cl- cotransport and the decrease of blood pressure after withdrawal was observed. In conclusion, chronic alcohol intake induces disturbances on red blood cell Na+ metabolism that dissipate with the cessation of drinking. Similar abnormalities also reported in humans and animals with primary hypertension have been associated in the pathogenesis of essential hypertension. Therefore, the pressor effect of chronic alcohol intake could be mediated through these changes in cellular Na+ metabolism.

Adolescent↗
PubMed1991

Therapeutic response may be predicted by some clinical parameters in essential hypertensive patients.

Several clinical parameters have been studied in a sample of 211 essential hypertensives in order to determine their usefulness as predictors of therapeutic response. One hundred and twenty-four patients (58.8%) achieved normotension with monotherapy, whereas 87 hypertensives (41.2%) needed two or more drugs to control their BP values. Patients who required a combination of drugs exhibited higher levels of systolic and diastolic BP, higher frequency of acute severe hypertension before the beginning of treatment, a more advanced stage of hypertension, and higher plasma aldosterone levels when they were compared with those controlled with a single drug. Likewise, previous cardiovascular complications related to hypertension, enlargement of cardiac silhouette on chest x-ray films and left ventricular hypertrophy were more frequent in the former. By means of a logistic regression analysis, these last three parameters showed a significant relationship with the number of required drugs. We conclude that hypertensives exhibiting this clinical profile have a higher probability of requiring a combination of drugs in the pharmacological treatment of essential hypertension.

Adult↗
PubMed1989

Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients.

We measured the ouabain- and bumetanide-resistant Na+ efflux in Mg2+-sucrose medium (passive Na+ leak) in erythrocytes from 30 normotensive controls and 72 essential hypertensive patients. The mean values (+/- SEM) of the rate constant of Na+ leak (kpNa) were not significantly different between normotensives and hypertensives. Nevertheless, using the 95% confidence limits of the kpNa (in 10(-3).h-1) in the normotensive group as a cut-off point, 7 (9.7%) essential hypertensives exhibited increased values (58.96 +/- 10.12) when compared with the other 65 patients (23.86 +/- 0.74). revealing increased passive Na+ permeability in the former (leak "+" hypertensives). Na+ fluxes depending on the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport were also measured in fresh erythrocytes from the same 72 patients. Three of them (4.2%) exhibited decreased values of ouabain-sensitive Na+ efflux and 6 (8.3%) of bumetanide-sensitive Na+ efflux, while 8 patients (11.1%) showed increased values of Li+-stimulated Na+ efflux and, finally, 48 patients (59.7%) did not present any evident abnormality in these Na+ transport systems. No differences were observed between leak "+" hypertensives and the remaining 65 patients when both basal erythrocyte Na+ content and clinical parameters of hypertension were compared. However, Na+ efflux depending on the outward Na+-K+ cotransport was significantly higher in the leak "+" hypertensive subset (299.43 +/- 43.18 vs 181.52 +/- 10.76 mumol.(l cells.h)-1; P = 0.0078), suggesting a compensatory phenomenon. Enhancement of Na+ permeability detected in 3% to 16% of essential hypertensives may be implicated in the pathogenesis of primary hypertension.

Adult↗
PubMed1989

Clinical profiles and erythrocyte Na+ transport abnormalities of four major types of primary hypertension in Spain.

The interaction of three different Na+ transport systems (Na+-K+ pump, Na+-K+ cotransport and Na+-Li+ countertransport), with internal Na+ and the passive Na+ leaks, were measured in erythrocytes from 72 Spanish, essential hypertensive patients and 30 normotensive controls. According to the observed abnormalities in Na+ transport pathways, 93.1% of the patients were classified into the following subsets: 12 (16.7%) exhibited a decreased apparent affinity of Na+-K+ pump for internal Na+ (Pump "-" hypertensives); 20 (27.7%) showed a decreased apparent affinity of Na+-K+ cotransport for internal Na+ (Co "-" hypertensives); 27 (37.5%) showed an accelerated Na+-Li+ countertransport (Counter "+" hypertensives); and 5 (6.9%) exhibited an increased rate constant of passive Na+ leaks (Leak "+" hypertensives). Finally, 5 patients (6.9%) did not show any abnormality in their Na+ transport systems and 3 exhibited more than one. Moreover, distinctive clinical features were recognize in Co "-" and Counter "+" subsets. Blood pressure values were lower in the former and, conversely, Counter "+" hypertensives showed a higher prevalence of moderate or severe hypertension (65.5% vs. 32.6%; P = 0.0059) and higher values of stimulated plasma renin activity (1.63 +/- 0.52 vs. 0.81 +/- 0.15; P = 0.0443). Our results confirm the heterogeneity of Na+ transport abnormalities in essential hypertension and suggest that these subsets of hypertensives could represent clinical entities.

Adult↗
PubMed1989

Disturbances of transmembranous sodium transport systems induced by ethanol in human erythrocytes. An approach to the pressor effect of alcohol.

Several epidemiological and clinical studies have established a clear association between alcohol consumption and hypertension. The mechanism of the pressor effect of ethanol is not well understood. We studied the in vitro effects of increasing amounts of ethanol on different Na+ transport systems from human erythrocytes. Ethanol at concentrations higher than 32 mmol/L stimulated ouabain-sensitive Na+ efflux, the Na+ efflux depending on the Na+:Li+ countertransport and Na+ leak. At the same concentrations, ethanol inhibited bumetanide-sensitive Na+ efflux. We conclude that, with the exception of Na+-K+ pump, alcohol-induced alterations and those observed in erythrocytes from essential hypertensives may overlap. Therefore, alcohol consumption could potentiate those genetic abnormalities of Na+ transport and contribute to the pathogenesis of essential hypertension.

Antiporters↗
PubMed1988

Na+-Li+ countertransport in essential hypertension.

Several studies on Na+-Li+ countertransport have reported higher rates in essential hypertensive than in normotensives, with a distribution pattern which is dependent on racial and ethnic background. However, it is not well established whether this abnormality in Na+ transport is associated with an abnormal clinical setting. In the present study we have performed a kinetic analysis of the interaction of the Na+-Li+ countertransport system with internal Na+ in erythrocytes from a sample of 72 essential hypertensives and 30 normotensive controls. A significant increase in mean values of the maximal rate of Li+-stimulated Na+ efflux (Vmax; 375.1 +/- 23.8 versus 213.7 +/- 8.5 mumol/l cells per h; mean +/- s.e.m.; Mann-Whitney test: U = 500; P less than 0.0001), as well as in the apparent affinity constant for internal Na+ (KNa; 10.03 +/- 0.08 versus 6 +/- 0.4 mmol/l cells; Mann-Whitney test: U = 718; P less than 0.0079), were observed in essential hypertensives with respect to normotensives. Using the 95% confidence interval of Vmax in normotensives as the normal range, 29 (40.3%) of the essential hypertensives exhibited values above the normal upper limit. The maximal rate (Vmax) and the internal Na+ content required for half-maximal stimulation (K50%) of Na+-K+ ATPase and outward Na+-K+ cotransport, and the rate constant of Na+ leak (KPNa) in this subset were similar to the values observed in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗