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Biomedical subjects

A Coca

Publications and source records attributed to A Coca.

At least 55 records · Page 3Linked to original sources
PubMed1997

Trough-to-peak ratio and circadian blood pressure profile after treatment with once-daily extended-release diltiazem, 240 mg, in patients with mild-to-moderate essential hypertension.

Once-daily diltiazem extended-release 240 mg (Lacerol-HTA Retard) was evaluated for safety, efficacy, and trough-to-peak ratio in a multicenter open study by using 24-h blood pressure (BP) monitoring in mild-to-moderate essential hypertension. After a 4-week washout period, 30 patients (17 men, 13 women) aged 25-76 years, showing a mean daytime diastolic BP (DBP) >90 mm Hg, were treated with diltiazem-ER, 240 mg, given once daily for 8 weeks. Ambulatory BP monitoring was obtained at the end of a 4-week placebo run-in period and during the last week of treatment. A significant reduction of the mean values of clinical BP [161.6 +/- 16.2 to 151.2 +/- 15.6 mm Hg; p < 0.01 for systolic BP (SBP); and 101.1 +/- 4.8 to 93.3 +/- 9.2 mm Hg; p < 0.001 for DBP] was observed at the end of treatment in the group of 30 patients, with no significant changes in heart rate (77.1 +/- 9.9 to 73.1 +/- 11.1 beats/min; p = NS). Likewise, mean values of 24-h SBP, DBP, SBP-load, and DBP-load were significantly reduced. In the group of 21 responders, the average reduction at peak was -18.6 +/- 12.9 mm Hg for SBP and -14.7 +/- 9.5 mm Hg for DBP. The residual effect at trough was -12.2 +/- 14.7 and -8.1 +/- 10 mm Hg, respectively. The trough-to-peak ratio was estimated as 0.66 for SBP and 0.55 for DBP. Long-term variability expressed as the mean standard deviation of BP for the 24-h period was reduced in responders (16.2 +/- 4.3 to 14.6 +/- 2.7 mm Hg for SBP; p = 0.0395; and 12.1 +/- 2.7 to 10.7 +/- 2.5 mm Hg for DBP; p = 0.0019), although no changes were observed in the variation coefficient (10.58-10.57% for SBP and 12.88-12.87% for DBP). We conclude that once-daily diltiazem-ER, 240 mg, was effective and well tolerated. Blood pressure was controlled over the entire period of 24 h, preserving the circadian profile and reducing long-term variability in responders. The significant reduction of both BP values and long-term variability may have implications involving protection from end-organ damage in essential hypertension.

Adult↗
PubMed1997

Oral calcium supplementation reduces intraplatelet free calcium concentration and insulin resistance in essential hypertensive patients.

We evaluated the effect of oral calcium supplementation on blood pressure, calcium metabolism, and insulin resistance in essential hypertension. After receiving a standard diet with 500 mg of calcium per day during a 4-week period, 20 nondiabetic, essential hypertensive patients were randomized in a double-blind fashion to receive oral calcium supplementation (1500 mg of calcium per day) or placebo for 8 weeks. At the end of the 4-week period of low-calcium diet and after the 8-week period of intervention, we measured blood pressure (by both office and 24-hour ambulatory blood pressure monitoring), calcium-regulating hormones [urinary hydroxyproline and serum osteocalcin, parathormone, and 1,25(OH)2-vitamin D3], intraplatelet free calcium concentration, fasting plasma glucose and insulin levels, and the insulin-sensitivity index (euglycemic-hyperinsulinemic clamp). Compared with patients maintained at low calcium intake, essential hypertensive patients under oral calcium supplementation significantly reduced serum osteocalcin (from 22.2 +/- 1.9 to 17.9 +/- 2.0 micrograms/L; P = .0015), parathormone (from 4.20 +/- 0.38 to 3.30 +/- 0.36 pmol/L; P = .0003), and 1,25(OH)2-vitamin D3 (from 98.0 +/- 11.0 to 61.6 +/- 5.7 pmol/L; P = .0062). Likewise, we found a significant reduction in intraplatelet free calcium concentration (from 35.9 +/- 1.2 to 26.5 +/- 0.8 nmol/L; P = .0005) and fasting plasma insulin levels (from 71.8 +/- 5.9 to 64.6 +/- 6.2 pmol/L; P = .05) and a significant increase in the insulin-sensitivity index (from 2.89 +/- 0.77 to 4.00 +/- 0.95 mg.kg-1.min-1; P = .0007). None of these parameters were significantly modified in patients maintained at low calcium intake. Office and 24-hour mean values of systolic and diastolic blood pressure did not change after 8 weeks of oral calcium supplementation or placebo.

Administration, Oral↗
PubMed1996

Fluid, ionic and hormonal changes induced by high salt intake in salt-sensitive and salt-resistant hypertensive patients.

1. The aim of the study was to detect differences between salt-sensitive and salt-resistant hypertensive patients in the response of the renin-aldosterone axis, plasma noradrenaline and atrial natriuretic peptide to high salt intake. 2. Fifty essential hypertensive patients followed 2 weeks of a standard diet with 20 mmol of NaCl daily, supplemented by placebo tablets for the first 7 days and by NaCl tablets for the last 7 days, in a single-blind fashion. Salt sensitivity was defined as a significant rise (P < 0.05) in 24 h mean blood pressure obtained by ambulatory blood pressure monitoring from the low- to the high-salt period. Biochemical and hormonal measurements were performed on the last day of both periods. 3. Twenty-two (44%) patients fulfilled criteria of salt-sensitive hypertension, whereas the remaining 28 (56%) were considered salt-resistant. High salt intake promoted a significant decrease (P < 0.05) in plasma creatinine, potassium, glucose, cholesterol, low-density lipoprotein-cholesterol, triacylglycerols, uric acid and plasma renin activity, and a significant increase in plasma atrial natriuretic peptide and 24 h urinary calcium excretion. The direction of these changes did not differ between salt-sensitive and salt-resistant patients. Salt-resistant hypertensive patients exhibited a significant decrease in plasma aldosterone induced by high salt intake (from 446 +/- 35 to 226 +/- 35 pmol/l; P < 0.001), whereas this parameter was not significantly modified in salt-sensitive patients (from 485 +/- 76 to 364 +/- 83 pmol/l; P not significant). Salt-sensitive patients showed an increase in plasma noradrenaline after high salt intake (from 1.15 +/- 0.11 to 1.56 +/- 0.14 nmol/l; P < 0.05), whereas salt-resistant patients presented a decrease in this parameter (from 1.48 +/- 0.08 to 1.12 +/- 0.08 nmol/l; P < 0.05). The change in plasma noradrenaline was directly correlated with the change in mean blood pressure induced by high salt intake (r = 0.479; P = 0.003). 4. We conclude that the increase in blood pressure induced by high salt intake in salt-sensitive patients is associated with a stimulation of the sympathetic nervous system and a blunted decrease in plasma aldosterone. Conversely, changes in renal function, electrolyte excretion and plasma concentrations of atrial natriuretic peptide induced by high salt intake seem to be similar in both salt-sensitive and salt-resistant patients.

Aldosterone↗
PubMed1996

Erythrocyte sodium transport, intraplatelet pH, and calcium concentration in salt-sensitive hypertension.

We evaluated changes in erythrocyte sodium transport systems, platelet pH, and calcium concentration induced by low and high salt intakes in a group of 50 essential hypertensive patients classified on the basis of their salt sensitivity. Patients received a standard diet with 20 mmol NaCl daily for 2 weeks supplemented in a single-blind fashion by placebo tablets the first 7 days and NaCl tablets the following 7 days. Salt sensitivity, defined as a significant rise (P <.05) in 24-hour mean blood pressure obtained by ambulatory blood pressure monitoring, was diagnosed in 22 (44%) patients. The remaining 28 (56%) were considered to have salt-resistant hypertension. In the entire group of hypertensive patients, high salt intake promoted a significant increase (P <.05) in the maximal rate of erythrocyte NA(+)-Li(+) countertransport (from 271 +/- 19 to 327 +/- 18 microM/(L cells/h) and of the Na(+)-dependent HCO3(-)-CL(-) exchanger (from 946 +/- 58 to 1237 +/- 92 microM/L cells/h) as well as in platelet pH (from 7.15+/-0 0.01 to 7.19+/-0.02 and calcium concentration (from 49+/-2 to 57 +/-2 nmol/L). Depending on salt sensitivity, high salt intake promoted opposing changes in some of the sodium transport systems studied. Salt-sensitive patients increased the maximal rate of the erythrocyte Na(+)-K(+) pump (fom 7.0 +/- 0.4 to 8.8 +/- 0.4 mmol/(L cells/h), Na(+)-K(+)-Cl(-) cotransport (from 416 +/- 37 to 612 +/- 41 micromol/(L cells/h), Na(+)-Li(+) countertransport (from 248 +/- 20 to 389 +/- 17 micromol/(L cells/h) at the end of the high salt period. Conversely, salt-resistant patients decreased the Na(+)-K(+) pump (from 8.0 +/- 0.4 to 6.9 +/- 0.3 mmol/(L cells/h) and Na(+)-K(+)-Cl(-) cotransport (from 578 +/- 53 to 481 +/- 43 micromol/(L cells/h). We conclude that modulation of erythrocyte sodium transport systems by high salt intake depends on salt sensitivity. The Na(+)-K(+) pump, Na(+)-K(+)-Cl(-) cotransport, and Na(+)-Li(+) countertransport increase in salt-sensitive patients, whereas the activity of these sodium transport systems tends to decrease in salt-resistant patients. Independent of salt sensitivity, high salt intake promotes a significant increase in the erythrocyte Na(+)-dependent HCO3(-)-Cl(-) exchanger, platelet pH, and calcium concentration in essential hypertensive patients.

Adult↗
PubMed1996

Increased left ventricular mass in salt-sensitive hypertensive patients.

Clinical, biochemical and echocardiographic characteristics were evaluated from 50 essential hypertensive patients classified asccording to their salt-sensitivity status. Salt-sensitive hypertension was diagnosed by means of ambulatory blood pressure monitoring (ABPM) in 22 (44%) patients showing a significant increase in mean BP (P < 0.05) from a 7-day period of low salt (20 mmol NaCl/day) intake, to a 7-day period of high salt (260 mmol NaCl/day) intake. The remaining 28 (56%) patients were considered as having salt-resistant hypertension. Compared with salt-resistant patients, salt-sensitive ones showed an increased left ventricular mass index (P = 0.0118), septal (P = 0.0021) and posterior wall thickness (P = 0.0026), without differences in the internal diastolic diameter. Decreased values of HDL-cholesterol (P = 0.0475) and increased total cholesterol/HDL-cholesterol ratio (P = 0.0098) were also observed in the salt-sensitive, compared with the salt-resistant hypertensive patients. Age, gender, body mass index, systolic and diastolic BP, fasting plasma glucose, creatinine and uric acid did not differ between salt-sensitive and salt-resistant patients. We conclude that, at the same level of BP, salt-sensitive patients exhibit an increased prevalence of left ventricular hypertrophy and a worse lipid profile. These two aspects 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↗
PubMed1995

Effect of long-term antihypertensive therapy with angiotensin converting enzyme inhibitors on red cell sodium transport.

Several sodium transport abnormalities have been reported in erythrocytes from essential hypertensive patients. The possible modification of these parameters under antihypertensive treatment remains controversial. We have measured the maximal rates of the Na+/K+ pump, Na+/K+/Cl- cotransport, and Na+/Li+ countertransport and the rate constant of Na+ leak in erythrocytes from 22 essential hypertensive patient responders to angiotensin converting enzyme inhibitors quinapril or captopril, and from 17 patient nonresponders to these drugs. In the former group, sodium transport measurements were performed at the baseline placebo period and after 6 months of active treatment. The maximal rate of Na+/Li+ countertransport decreased significantly after 6 months of treatment, without differences between both groups of treatment. Angiotensin converting enzyme inhibitors did not significantly modify other sodium transport parameters. The basal activity of erythrocyte sodium transport was not different between patients who responded or not to antihypertensive treatment with those drugs, excluding a predictive value of these measurements concerning the response to angiotensin converting enzyme inhibitors.

Adult↗
PubMed1995

Detection of a circulating inhibitor of the Na(+)-K(+)-Cl(-) cotransport system in plasma and urine after high salt intake.

The aim of the study was to detect the presence of an endogenous Na(+)-K(+)-Cl- cotransport inhibitor factor in plasma and urine from salt-loaded subjects. Twenty-six essential hypertensive patients (13 men, 13 women) and 6 normotensive controls (2 men, 4 women) received a diet containing 260 mmol/day of NaCl tablets for 7 days. Human erythrocytes from healthy blood donors (using bumetanide-stimulated Li+ efflux) were used to test the inhibition of Na(+)-K(+)-Cl- cotransport by different plasma and urine concentrations collected the last day of the salt-loaded period. The addition of plasma and urine from salt-loaded subjects significantly inhibited erythrocyte Na(+)-K(+)-Cl- cotransport (P < .001). No differences were observed between hypertensive patients and normotensive controls. These results provide evidence of an Na(+)-K(+)-Cl- cotransport inhibitor factor in plasma and urine from salt-loaded humans, in concordance with previous reports in salt-loaded rats.

Adult↗
PubMed1995

Assessment of salt sensitivity in essential hypertension by 24-h ambulatory blood pressure monitoring.

We used ambulatory blood pressure monitoring (ABPM) in the assessment of salt sensitivity in 40 essential hypertensive patients, comparing 24-h mean blood pressure during 7 days of low salt (20 mmol NaCl/day) and high salt (260 mmol NaCl/day) intake. Salt sensitivity was diagnosed in 18 essential hypertensive patients (45%), each of them showing a significant increase in mean blood pressure (P < .05) from low to high salt diet. Salt-sensitive patients exhibited a high-salt-dependent increase in all blood pressure parameters including 24-h systolic, mean, diastolic blood pressure, blood pressure load, area under the curve, and awake and asleep blood pressure values. These patients exhibited a nondipper profile on both low-salt and high-salt diets. Salt-resistant patients (55%) showed a decrease in awake, and an increase in asleep blood pressure values after high salt intake, thus tending to flatten the circadian blood pressure profile. We conclude that ABPM is a useful method to assess salt sensitivity. In salt-resistant patients high salt intake induces a significant increase in asleep blood pressure with no significant changes in 24-h blood pressure, promoting a flattened blood pressure curve and tending to transform a dipper into a nondipper profile, which could have important implications in end-organ damage.

Adult↗
PubMed1995

Haemophilus paraphrophilus endocarditis: case report and review.

Endocarditis due to Haemophilus paraphrophilus is an uncommon disease. We report a case of H. paraphrophilus endocarditis with embolic complications in which the causative organism was resistant to beta-lactam antibiotics. Before April 1994, 16 cases of H. paraphrophilus endocarditis had been reported. Infection by this organism usually affects a previously damaged mitral valve. We emphasize the fastidiousness of the organism and the high incidence of embolic complications, which determine the outcome. To our knowledge we describe the first patient with endocarditis due to beta-lactam-resistant H. paraphrophilus.

Adult↗
PubMed1995

Increased plasma endothelin concentration in atherosclerotic renovascular hypertension.

The aim was to investigate circulating levels of immunoreactive endothelin (ir-ET) in atherosclerotic renovascular hypertension (RVH), and to assess the role of the kidneys in its overall plasma concentration. We studied 16 hypertensive patients with renal artery stenosis evidenced by angiography and admitted to hospital for the diagnostic evaluation of RVH by renal vein plasma renin activity (PRA) determinations. The right femoral vein was catheterized to simultaneously measure PRA and ir-ET in both renal veins and inferior vena cava below the origin of the renal veins. RVH was present in 9 patients as indicated by diagnostic PRA renal vein ratios and the remaining 7 patients were considered to have essential hypertension (EH). Patients with RVH showed a marked increase in systemic plasma ir-ET concentration (10.3 +/- 0.9 pg/ml). Despite a significant increase of PRA in the vein of the ischemic (IK) versus the contralateral (CK) kidney in patients with RVH, no significant differences in ir-ET concentration were observed between both kidneys. These results indicate that patients with RVH have increased circulating levels of ir-ET. However, the higher systemic plasma ir-ET do not arise from the renal circulation, since plasma ir-ET is significantly higher in systemic circulation than in renal veins.

Creatinine↗
PubMed1994

Increased activity of the Mg2+/Na+ exchanger in red blood cells from essential hypertensive patients.

Epidemiological, clinical, and experimental evidence suggests a relation between Mg2+ metabolism and essential hypertension. The aim of the present study was the detection of abnormalities of the erythrocyte Mg2+/Na+ exchanger in essential hypertensive patients. We studied 66 untreated essential hypertensive patients and 36 normotensive control subjects. Maximal efflux rates of total Mg2+ efflux and the Na(+)-dependent and Na(+)-independent components of Mg2+ efflux were determined in Mg(2+)-loaded red blood cells. Mg2+/Na+ exchanger was calculated as the Na(+)-dependent component of the Mg2+ efflux. Mean values of Mg2+/Na+ exchanger were clearly elevated in hypertensive subjects with respect to normotensive control subjects [184.7 +/- 15.7 versus 84.4 +/- 6 mumol(L.cell.h)-1; P < .001]. This elevation was due primarily to the increased total Mg2+ efflux [324.2 +/- 21.9 versus 257.9 +/- 17.3 mumol(L.cell.h)-1; P < .05], whereas the Na(+)-independent component was not significantly different between the groups [154.5 +/- 11.8 versus 173.4 +/- 15.5 mumol(L.cell.h)-1; P = NS]. Moreover, total erythrocyte Mg2+ content was slightly reduced in hypertensive patients with respect to normotensive control subjects (1.84 +/- 0.04 versus 2.07 +/- 0.04 mmol/L.cell; P < .001). Using the 99% confidence limits of the normotensive population as the normal range, 30 (45.5%) hypertensive subjects showed values of Mg2+/Na+ exchanger higher than 160 mumol(L.cell.h)-1. The Mg2+/Na+ exchanger was inversely correlated with basal intraerythrocyte Mg2+ content (r = -.323; P = .001). From a clinical point of view, we found a positive correlation between diastolic blood pressure values and Mg2+/Na+ exchanger (r = .246; P < .05) in the sample of essential hypertensive patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Circadian rhythm and blood pressure control: physiological and pathophysiological factors.

AIM: To review current knowledge on blood pressure variability. BLOOD PRESSURE VARIABILITY: Blood pressure variability has a time-course ranging from a few seconds or minutes (short-term variability) to 24 h (long-term variability) or 1 year (seasonal variations). The variability is influenced by physiological factors such as physical and mental activity (posture, exercise, talking) or behavioral and environmental factors (salt, caffeine, alcohol), and by pathological conditions. In patients with essential hypertension, the day-night pattern of blood pressure change is generally similar to that of normotensives, with a significant nocturnal blood pressure fall (dippers), except that the entire profile is shifted upwards. Nevertheless, in some essential hypertensives the nocturnal fall in blood pressure is absent or reversed (non-dippers), in spite of a decrease in the nocturnal heart rate. In several forms of secondary hypertension (pheochromocytoma, renal failure) and other clinical conditions (sleep apnea syndrome, diabetes mellitus, cardiac transplantation) the nocturnal fall in blood pressure is also absent or reversed. CONCLUSIONS: Blood pressure variability and the blunted nocturnal fall in blood pressure may be clinically relevant. Several studies have demonstrated that subjects whose 24-h variability was higher than the group average were more likely to have target-organ damage. Moreover, hypertensive women with a blunted nocturnal fall in blood pressure (non-dippers) are more likely to suffer morbid cardiovascular events than dippers. On theoretical grounds, therefore, antihypertensive treatment that reduces blood pressure variability and preserves the nocturnal fall in blood pressure will help to protect target organs in hypertension. So far, this has not been demonstrated in clinical trials.

Antihypertensive Agents↗
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↗