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Biomedical subjects

A J Ramírez

Publications and source records attributed to A J Ramírez.

14 recordsLinked to original sources
PubMed2002

Higher urinary albumin excretion is associated with abnormal erythrocyte Na(+)/Li(+) countertransport (SLC) in non-modulating essential hypertensives and offspring of hypertensive parents.

Non-modulating is a highly reproducible type of sodium-sensitive hypertension. The aim of this study was to evaluate in non-modulating individuals the erythrocyte sodium-lithium countertransport (SLC) abnormalities, which have been mentioned as a marker of non-modulation, and the association with increased microalbuminuria, as a marker of an early kidney impairment. We measured erythrocyte SLC in 10 normotensives (NT, 28 +/- 4 years), 20 offspring of hypertensive parents being 10 modulating (MHO, 25 +/- 6 years) and 10 non-modulating (NMHO, 26 +/- 5 years), and 23 essential hypertensives being 12 modulating (MHT, 34 +/- 5 years) and 11 non-modulating (NMHT, 32 +/- 4 years). In all the subjects studied, microalbuminuria was determined by duplicate 24-h urine collection by radioimmunoassay. In non-modulating offspring of hypertensive parents and essential hypertensives. SLC was significantly elevated when compared either with normotensives without family history of hypertension, modulating offspring of hypertensive parents or essential hypertensives (P < 0.025). Likewise, 24-h urinary albumin excretion was found higher in non-modulating individuals (essential hypertensives and offspring of hypertensive parents) than in modulating individuals (P < 0.01). In conclusion, non-modulators with higher SLC countertransport sodium transport abnormalities showed higher elimination of microalbuminuria suggesting that non-modulators may have an increased risk for developing cardiovascular morbidity and kidney impairment even in normotensive subjects with familiarity history of hypertension.

Adult↗
PubMed2001

The metabolic syndrome and related cardiovascular risk.

The metabolic syndrome is a complex association of several risk factors including insulin resistance, dyslipidemia, and essential hypertension. Insulin resistance has been associated with sympathetic activation and endothelial dysfunction, which are the main mechanisms involved in the pathophysiology of hypertension and its related cardiovascular risk. According to the Sixth Report of the Joint National Committee, and guidelines of the World Health Organization/International Society of Hypertension, the presence of multiple risk markers suggests that both hypertension and risk factors should be aggressively managed in order to obtain a better outcome. Primary prevention of obesity at different levels--individual, familial, and social-- starting early in childhood has proven to be cost effective, and will be mandatory to reduce the world epidemic of obesity and its severe consequences.

Cardiovascular Diseases↗
PubMed2001

Mechanical vs intrinsic components in the improvement of brachial arterial compliance. Comparison of the effects of atenolol versus ramipril in hypertensive patients.

The aim of this study was to compare the mechanical and intrinsic effects of an angiotensin converting enzyme inhibitor, vs a beta-blocker, on brachial arterial compliance. In a double blind study, 34 essential hypertensive patients were treated for 3 months with either ramipril 2.5-5.0 mg daily (n = 17, age 57 +/- 7 y, 11 males) or atenolol 50-100 mg daily (n = 17, age 53 +/- 8 y, 11 males). Blood pressure (BP), brachial artery diameter (D), brachial-radial pulse wave velocity (PWV) and effective compliance (Ceff), were measured before and at the end of the study. Isobaric evaluation (Ciso) was performed in the entire population studied at an average mean BP of 110 mmHg. Ramipril significantly reduced BP from 155 +/- 16/94 +/- 6 mmHg to 140 +/- 15/85 +/- 7 mmHg (p < 0.001) without affecting heart rate (HR; 74 +/- 10 vs. 75 +/- 12 bpm). In addition, it significantly improved both PWV (18%; p < 0.001) and arterial compliance (45%; p < 0.001), from which 35% was related to a pressure independent effect (p < 0.01). Atenolol also induced a reduction in both BP (159 +/- 17/96 +/- 10 to 133 +/- 13/81 +/- 8 mmHg; p < 0.001) and HR (76 +/- 10 to 57 +/- 7 bpm; p < 0.001). In a similar way, PWV (11%; p < 0.05) and Ceff (30%; p < 0.05) were significantly improved without significant change in Ciso. This suggests that blood pressure reduction was responsible for compliance improvement. In conclusion, it is suggested that atenolol induces only hemodynamic changes, mediated mainly by BP reduction. In contrast, the improved brachial buffering function observed after ramipril involves not only hemodynamic changes, but also changes mediated by other mechanisms, such as modification of wall structures.

Adrenergic beta-Antagonists↗
PubMed1997

Erythrocyte sodium-lithium countertransport in non-modulating offspring and essential hypertensive individuals: response to enalapril.

Non-modulators are a subset of essential hypertensive individuals in whom renal hemodynamic and adrenal aldosterone responses to angiotensin II fail to modulate appropriately during high dietary salt intake. The main aim of this study was to investigate the familial aggregation of non-modulation and several erythrocyte Na+ transport systems in normotensive and hypertensive individuals as well as offspring of hypertensive parents. An additional aim was to evaluate the effect of treatment with enalapril on erythrocyte Na+ transport. We studied 15 normotensive subjects (6 males, 27+/-6 years), 14 untreated modulating essential hypertensive subjects (7 males, 38+/-7 years), 12 untreated non-modulating essential hypertensive subjects (7 males, 38+/-6 years), 14 modulating offspring of hypertensive parents (8 males, 25+/-6 years), and 14 non-modulating offspring of hypertensive parents (8 males, 26+/-4 years). Blood pressure was recorded with an oscillometric device and renal plasma flow and glomerular filtration rate by clearances of para-aminohippurate and inulin, respectively. Non-modulating subjects were identified as individuals who failed to increase effective renal plasma flow by 30% and decrease filtration fraction by at least 30% 10 days after changing from a low (20 mmol/d) to a high (250 mmol/d) sodium intake. Erythrocyte Na+ transport was characterized by measurements of the Na+-K+ pump, Na+-Li+ countertransport, Na+-K+-Cl- cotransport, passive Na+ permeability, and Na+ content. After the initial studies, hypertensive individuals were treated with enalapril (20 mg/d P.O.) for 6 months, after which erythrocyte Na+ transport measurements were again made. The main findings were that Na+-Li+ countertransport is increased in non-modulating hypertensive subjects and non-modulating offspring of hypertensive parents, that the increase in blood pressure in response to high salt intake is greater in non-modulating than modulating hypertensive subjects, and that enalapril decreases Na+-Li+ countertransport activity to normal in non-modulating hypertensive subjects. These findings provide support for a possible genetic role in the development of salt sensitivity and suggest that Na+-Li+ countertransport and non-modulation are related phenotypes.

Adult↗
PubMed1993

Psychiatric disorder in patients with advanced breast cancer: prevalence and associated factors.

The prevalence of psychiatric disorder and associated factors has been examined in 139 women with advanced breast cancer. Patients completed a self-report assessment of mood, the Hospital Anxiety and Depression Scale (HAD). They were also interviewed to obtain sociodemographic details, UICC performance status and past psychiatric history. Overall, 35 (25%) scored 11 or above (out of a maximum of 21) on either the anxiety or the depression subscales, or both, of the HAD and were therefore probable cases of anxiety and/or depression. These patients are likely to benefit from psychosocial intervention. Clinical anxiety was unrelated to any sociodemographic or disease related factors. Clinical depression was significantly more prevalent amongst patients in the lower socioeconomic classes (P = 0.01) and those with poor performance status (P = 0.007). Depression can be difficult to detect in patients with advanced breast cancer and these factors may be useful indicators to clinicians of patients at high risk of this disorder.

Adult↗
PubMed1992

Early abnormalities of left ventricular function in essential hypertension induced by exercise.

In order to assess their ventricular function at rest and during exercise, 42 essential hypertensives (164 +/- 2/98.7 +/- 2 mmHg) and 12 normotensives (131.7 +/- 4/81.2 +/- 1 mmHg) were studied. Ejection fraction (EF), peak filling rate (PFR) and peak ejection rate (PER) were measured by means of gated radionuclide ventriculography. At rest, no differences in EF, PFR and PER between hypertensives and normotensives were found. During exercise, hypertensives showed lower PFR (5.3 +/- 0.2 EDV/s) and EF (67.7 +/- 1%) than normotensives (PFR 7 +/- 0.5 EDV/s, p < 0.005 and EF 79.4 +/- 2%, p < 0.001). Likewise, hypertensive showed a lower increase from rest to exercise in PFR and in EF than normotensives p < 0.001. In addition, hypertensives showed a great individual variability in EF response to exercise, where 23 patients increased EF more than 5% and 19 patients failed to increase it during stress. Moreover, the last group of patients had higher systolic blood pressure (SBP) both at rest and during exercise than patients who increased EF, p < 0.01. In addition, there was a significantly negative correlation between resting SBP and the variation of Ef (r = 0.47 y: 163.1-0.79X, p < 0.01). Left ventricular mass (LVM) was similar in the two groups of hypertensives. On the other hand, there were no differences in any of the variables analyzed between the hypertensives with LV hypertrophy and those with normal LVM. These findings suggest that abnormalities in both systolic and diastolic LV during exercise may be found in hypertensive patients even before myocardial hypertrophy can be detected.

Adult↗
PubMed1991

Effects of ACE inhibition on renal haemodynamics in essential hypertension and hypertension associated with chronic renal failure.

Angiotensin II has many actions in the kidney, including regulation and distribution of renal circulation and glomerular filtration, as well as effects on mesangial contraction and on the filtration coefficient. The reduction in circulating and intrarenal angiotensin II by angiotensin converting enzyme (ACE) inhibitors in essential hypertension is associated with a significant increase in renal blood flow and a decrease in filtration fraction, without changes in glomerular filtration rate. In addition, administration of ACE inhibitors can reduce proximal sodium reabsorption via changes in peritubular hydrostatic and oncotic forces resulting from the fall in postglomerular capillary resistance. In severe hypertension the state of the renal vasculature does not allow ACE inhibition to induce similar haemodynamic changes and, therefore, it cannot contribute to renal sodium handling that requires the recruitment of alternate mechanisms. In spite of this, ACE inhibitors may exert a protective effect on the renal function of patients with severe hypertension as well as in those with renal impairment, by lowering systemic and, probably, intraglomerular pressure, reducing proteinuria and slowing the progression of renal failure.

Adolescent↗
PubMed1990

Analysis of left ventricular function by radionuclide ventriculogram in hypertensive patients treated with atenolol.

The myocardial effects of a daily oral dose of atenolol were studied by radionuclide multi-triggered ventriculogram in 10 patients (7 men and 3 women) with mild to moderate essential hypertension, aged 29 to 53 years (mean 43) at rest and during exercise. Before and after two months of treatment with 100 mg/day orally of atenolol, the following variables were recorded: systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), ejection fraction (EF), peak filling rate (PFR) and peak ejection rate (PER). Beta-blockade treatment caused a significant drop in SBP and DBP, both at rest and during exercise; HR slowed down at rest and during exercise. PFR diminished at rest and during exercise. PER was reduced at rest and during exercise (p less than 0.001). No significant changes in EF were observed after treatment with atenolol. In conclusion, atenolol impaired left ventricular relaxation in spite of the drop in blood pressure.

Adult↗
PubMed1989

[Automated ambulatory 24-hour monitoring of blood pressure in hypertensive patients].

In order to analyse the 24 h blood pressure pattern, a non-invasive 24 h ABPM was recorded in 18 normotensives (23-44 years) and in 24 untreated essential hypertensives (28-65 years) using a Space-Labs 90202. This device was previously validated with a mercury sphigmomanometer (S) and with intraarterial blood pressure (IA). The correlation coefficient obtained for systolic blood pressure (SBP) between ABPM and IA was 0.89, p less than 0.0001 and between ABPM and S was 0.98, p less than 0.0001. Likewise, a significative correlation for diastolic blood pressure (DBP) was found between ABPM and IA (r = 0.78, p less than 0.0001) and between ABPM and S (r = 0.97, p less than 0.0001). Essential hypertensives showed higher mean values of SBP and DBP than normotensives (p less than 0.01) maintaining a similar circadian pattern. In these patients, the percentages of mean abnormal SBP (greater than 140 mmHg) and DBP (greater than 90 mmHg) readings were greater than 58% and 56% for the 24 h period, and 70% and 77% for the activity period, respectively. On the other hand, in normotensives the percentages of mean abnormal SBP and DBP readings were lower than 10.5% and 5.7% for the 24 h period, and 17.2% and 11.7% during the activity period, respectively. In conclusion, 24 h ABPM enabled us to characterize two well differentiated populations either by mean BP values of the percentages of abnormal readings. Between normotensives and hypertensives an intermediate group of subjects, with normal mean BP values and higher percentages of abnormal BP readings than normotensives remains to be characterized and longitudinally studied in order to evaluate their target organ repercussion.

Adult↗
PubMed1982

Central serotonergic participation on blood pressure regulation.

1. The changes on blood pressure induced by pharmacological handling of serotonergic systems were studied in normotensive anesthetized rats. Administration of 5-hydroxytryptophan (5-HTP) (5, 10 and 30 mg/kg i.v.) produced a dose-dependent decrease in mean blood pressure without significative effect on heart rate. 2. Inhibition of either peripheral L-aminoacid DOPA decarboxylase or monoamine oxydase enzymes increased this hypotensive effect. 3. Methysergide, a serotonergic antagonist, prevented the hypotension induced by 5 OH-TP in animals whose peripheral decarboxylase was inhibited. 4. Fenfluramine, a serotonergic releasing drug, produced a decrease in both blood pressure and heart rate. These effects were prevented by inhibiting fenfluramine uptake or by serotonin (5-HT) receptor blockade. 5. The hypotensive action induced by 5-HTP was not affected when opioid, dopaminergic or histaminergic receptors were blocked. 6. In animals injected intracisternally with a serotonergic neurotoxine a selective destruction of serotonergic terminals of spinal cord was obtained. 7. In these animals the dose-response curve relating hypotensive effect induced by a direct serotonergic agonist showed a significative shift to the left when compared with control group, suggesting the existence of supersensitivity. 8. Our results show that increases in central serotonergic activity produce a hypotensive effect in normotensive anesthetized rats. The receptor involved in this action could be localized in spinal cord.

5,7-Dihydroxytryptamine↗
PubMed1980

Sinoaortic denervation-induced changes in central serotonergic neurons.

Sinoaortic denervation in rats induced changes in endogenous levels of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) in brain areas. The midbrain showed a sustained increase for 7 days after the operation, while in pons and medulla oblongata a marked rise was only observed during the first 24 h. No changes were obtained in spinal cord. It is thought that the changes in serotonergic activity described could be related to the neurogenic hypertension induced by sinoaortic denervation.

Animals↗
PubMed1980

Blood pressure and heart rate response to apomorphine in urethane anesthetized rats.

The mechanisms involved in the hypotensive effect of apomorphine were studied in urethane anesthetized rats. The intravenous injection of apomorphine (0.01-0.75 mg/kg) produced a dose dependent fall in mean blood pressure. At the higher doses used (0.5-0.75 mg/kg) a marked bradycardia accompanied the hypotensive effect. These cardiovascular effects were prevented by pretreating the animals with pimozide (0.01-0.1 mg/kg). Low doses of haloperidol (0.03-0.3 mg/kg) did not antagonize the hypotensive action of apomorphine. Higher doses of haloperidol (1-3 mg/kg) reduced markedly the mean blood pressure. Atropine (1 mg/kg) partially antagonized the decrease in mean blood pressure induced by apomorphine and prevented completely the bradycardia. Hexamethonium (10 mg/kg) reduced the mean blood pressure and when apomorphine was administered, a residual hypotensive effect and no bradycardia was observed. It is concluded that the cardiovascular actions of apomorphine are central in origin and mainly due to the stimulation of a dopamine receptor. A probable peripheral effect could not be discarded.

Animals↗