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C Posadas

Publications and source records attributed to C Posadas.

17 recordsLinked to original sources
PubMed1986

Effect of pertussis toxin on the heart muscarinic-cholinergic receptors and their function.

Administration of pertussis toxin to rats induced a significant increase in heart rate that was evident as soon as 24 hours after the administration of the toxin and that persisted for at least 15 days. Electrical stimulation of the vagus decreased dramatically the heart rate of control animals but was unable to do it so in rats treated with pertussis toxin. In cardiac membranes muscarinic agonists decreased adenylate cyclase activity (approximately equal to 20-25%); no effect was observed in membranes obtained from toxin-treated animals. Agonist displacement of antagonist binding [( 3H] Quinuclidinyl benzilate) indicated that treatment with pertussis toxin decreased the proportion of receptors in the high affinity state for agonists. All these data suggest that blockade of the parasympathetic tone plays a key role in the induction of tachycardia by pertussis toxin.

Adenylate Cyclase Toxin↗
PubMed1986

Effect of pertussis toxin on the heart acetylcholine muscarinic receptor affinity.

The effect of pertussis toxin on the affinity for agonists and antagonists of the heart muscarine acetylcholine receptor was studied using the radiolabeled antagonist [3H]quinuclidinyl benzylate ([3H]QNB). In cardiac membranes from control rats the displacement of [3H]QNB by carbachol was consistent with two classes of binding sites, kDH 25 +/- 10 nM and kDL 3,006 +/- 869 nM. The proportion of sites in the high and low affinity state for agonists was 55 and 45% respectively. In the presence of 100 microM guanyl-5'-yl imidodiphosphate (Gpp(NH)p), only the low affinity state for agonists was observed (kDL 3,804 +/- 759 nM). In cardiac membranes from pertussis toxin-treated rats, two classes of binding sites with affinities similar to those seen in the controls were also observed in the absence of guanine nucleotide (kDs 39 +/- 12 and 3,315 +/- 845 nM) but the proportion of sites were 20 and 80% for high and low affinity respectively. Gpp(NH)p shifted the remaining 20% of sites from the high affinity to the low affinity state (KD 4,093 +/- 744 nM). The receptor KD for antagonists was decreased by pretreatment with pertussis toxin from 83 +/- 7 to 56 +/- 5 pM (P less than 0.01); Gpp(NH)p induced a further change in the affinity for the antagonist in membranes from both control and pertussis toxin-treated rats. The change suggested positive cooperativity. The total number of sites was not modified significantly by either pertussis toxin treatment or guanine nucleotides. These results are consistent with a possible reciprocal modulation of the affinity for agonists and antagonists of the cardiac muscarine receptor.

Animals↗
PubMed1986

Guanine nucleotide-induced positive cooperativity in muscarinic-cholinergic antagonist binding.

The effect of guanine nucleotides on the binding of [3H] Quinuclidinyl benzilate to heart muscarinic receptors was studied. It was observed that GTP and Gpp (NH)p increased antagonist binding. Scatchard transformation of the data resulted in curvilinear plots (downward concavity) consistent with positive cooperativity. Graphic analysis for cooperativity indicated that guanine nucleotides: a) increased slightly but consistently the affinity for the antagonist (independent of receptor occupancy) and b) induce positive cooperativity in the binding of [3H]QNB (dependent of receptor occupancy).

Animals↗
PubMedDate not supplied

[Premature atherosclerosis in a 17-year-old male with diabetes mellitus and familial dyslipoproteinemia].

A 17-year-old male was admitted with an acute myocardial infarction. A coronarography showed 90% occlusion in of the descendent anterior artery. A coronary angioplasty was done with excellent response. As coronary risk factors he had diabetes mellitus for 5 years and dyslipidemia with a phenotype IIb and hypo-alpha-lipoproteinemia. The case is discussed in regard to the possible etiopathogenic causes for his premature atherosclerosis.

Adolescent↗
PubMedDate not supplied

[Effects of aerobic physical conditioning on the profile of plasma lipoproteins in a group of healthy volunteers].

To evaluate the effects of aerobic physical conditioning on plasma lipoproteins, we studied 26 previously untrained, apparently healthy, non obese volunteers. All participants underwent a treadmill test performed according to the protocol of Bruce with the direct measurement of maximal oxygen consumption (VO2max). A program of aerobic exercise was prescribed for each volunteer at 70% of their corresponding VO2max. At baseline and at the end of weeks 4, 8 and 12 of the exercise program, cholesterol and triglycerides were measured by enzymatic analysis in total plasma and in the lipoprotein fractions separated by preparative ultracentrifugation and precipitation methods. At the end of week 12, the VO2max measurement was repeated. At the end of the protocol, mean VO2max increased from the value of 39.9 observed at baseline to 94.4 ml/kg/min (p less than 0.01). There were no variations in mean body weight, diet or smoking status of the participants during the exercise program. Cholesterol associated with High-density lipoproteins (C-HDL) increased from 42.5 to 46.1 mg/dl (p less than 0.05). This effect was first noticeable at week 8. We didn't observe significant changes in Total Cholesterol nor the Cholesterol fraction associated with Low-density lipoproteins (C-LDL). Total triglycerides decreased at weeks 4 and 8 but returned to near baseline values at week 12. The C-LDL/C-HDL ratio considered as an index of a high coronary risk decreased from 2.32 at baseline to 2.02 (p less than 0.05) at week 12. Thirteen of the twenty six initial volunteers completed the physical conditioning program as planned, the rest were eliminated at different stages of the protocol due to incomplete adherence to their exercise schedules.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Perioperative management of the diabetic patient in cardiac surgery with extracorporeal circulation].

The hyperglycemia usually observed in patients undergoing heart surgery with extracorporeal circulation (EC) represents a difficult therapeutic problem. We studied the effects of several regimens of insulin therapy on serum glucose (SG) in 24 noninsulin dependent diabetic patients (NIDDs). The patients were randomly divided in five groups; group A received on IV bolus of 10.0-50.0 U/h according to glycosuria; groups B, C, D and E were given a continuous iv insulin infusion of 2.5, 5.0, 7.5 and 10.0 U/h respectively. In 10 non-diabetic patients (NDP) SG levels were also measured, but insulin was not given. A mean of 5.0 l/m2 of body surface of fluids containing 300 g of glucose were administered to all patients during surgery. At the operations SG levels rose progressively soon after the anesthesia was started, reached the highest values during the period of EC, and decreased slowly in blood samples taken after the EC phase and by 24h. This patterns was shown by all groups studied statistically significant lower SG levels, however, were observed in patients of group C, whose values were similar to those seen in the NDP group. Groups D and E had slightly higher SG levels than those of group C. An additional NIDDM patient with advanced chronic renal failure (CRF), had a tendency to hypoglycemia even during the EC period in response to relatively low doses of insulin (2.5 U/h), given by a continuous iv infusion and, although the insulin administration was stopped, his SG levels remained well below the mean values of the other patients for the rest of the operation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Thyroid dysfunction induced by amiodarone].

Amiodarone (2-n-butyl-3,4-diethylaminoethoxy-3',-diiodobenzoyl-benzofurone ) is a drug widely used for the treatment of cardiac arrhythmias. Due to its high iodine content and structural similarity to thyroxine it produces abnormalities in thyroid hormone metabolism and, in some cases, clinical thyroid dysfunction as well. We report 18 patients, 11 females and 7 males, whose thyroid disease developed during treatment with amiodarone (A). Age ranged from 13 to 64 years. A history of thyroid disease in a first-degree relative was present in five, and three patients had goiter prior to A therapy. Fifteen patients had atrial arrhythmias, and 3 had ventricular arrhythmias. Amiodarone was being given in doses of 200 to 800 mg daily. Thyroid function abnormalities appeared between 1 and 29 months after starting A therapy. Nine patients became clinically and chemically thyrotoxic; three patients developed diffuse thyroid enlargement and had total T4 concentration and FI4I increased with normal T3 and no signs of hyperthyroidism; and the six remaining patients became clinically hypothyroid with low values of total T4 and FTI and raised basal TSH. No relationship between dosages of A or duration of treatment and the appearance or severity of thyroid dysfunction was found. Regression of symptoms occurred in all but two patients with simple goiter between 1 and 8 months after amiodarone was discontinued and appropriate treatment was given. Our observations confirm the potential of A to induce thyroid abnormalities in patients with and without preexistent thyroid disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

[Evaluation of sympathetic tone in essential hypertension by the clonidine suppression test].

Recent evidences suggest that the sympathetic nervous system plays a major role in the pathogenesis and maintenance of several clinical forms of hypertensive disease. The clonidine suppression test allows us to uncover the subtle changes in neuronal noradrenaline release in essential hypertension. To prove this possibility, we selected 16 patients: 7 borderline hypertensives (BH) (4 males and 3 females), mean age: 24 years; and 9 established hypertensives (EH) (6 males and 3 females), mean age: 25 years. In both groups, the heart rate (HR) and blood pressure (BP) were registered every 30 min and by intravenous catheter plasma catecholamines (PCA) and plasma renin activity (PRA) were measured before and after (180 and 240 min) one oral dosis of clonidine (300 mcg) had been administered. Patients remained in clinostatism for 180 and and orthostatism for 60 min. HR and BP diminished in BH and EH after clonidine during clinostatism in comparison to preclonidine period. PCA also showed reduction in 180 min with respect to the basaline period. PRA did not present change in 180 min in either groups in relation to time O. During orthostatism, HR increased in both groups with respect to the baseline period. BP remained low in relation to baseline time. PCA were increased with respect to preclonidine period. PRA showed a slight tendency to increase in relation to time O in both groups. CAP baseline level are not reliable indexes of the role of the sympathetic tone in maintenance of high BP values in hypertensive disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Autoimmunity in thyroid disease secondary to amiodarone: heredofamilial aspects].

Spontaneous autoimmune thyroid disease (SATD) shows familial aggregation. Some patients receiving amiodarone treatment have been found to develop thyroid dysfunction. Previously, we reported genetic predisposition among this group of patients, now we inform a prospective study which includes the search for autoantibodies and family history to identify risk factors in amiodarone treated patients, 40 of them with amiodarone related thyroid disfunction, and 100 without it; for comparison, 30 patients with SATD and a control group of healthy subjects were also studied. We looked for the presence of autoantibodies against thyroglobulin, smooth muscle, gastric mucosa, myocardium, mitochondria, epithelial intercellular substance, and basal membrane as well as antinuclear antibodies and rheumatoid factors; in addition the history of thyroid disease in first degree relatives was investigated. Organ-specific antibodies anti-thyroglobulin, gastric mucosa and myocardium were found with increased frequency in the three groups of patients compared with controls (p less than 0.05). The frequency of antihydroglobulin antibodies was similar in patients receiving amiodarone with or without thyroid dysfunction. Prognostic stratification revealed that this finding is independent of sex, age, dosage or duration of treatment. A family history of thyroid dysfunction was found more frequently among patients with SATD and amiodarone related dysthyroidism in comparison with patients receiving amiodarone without altered thyroid function (p less than 0.005). The appearance of clinical thyroid disease depends on individual genetical predisposition. In patients with a positive family history, the risk of developing clinical, thyroid disease is 7.6 when treated with amiodarone.

Adolescent↗
PubMedDate not supplied

[The renin angiotensin system in the pathology of arterial hypertension of aortic coarctation].

Nine patients with aortic coarctation were studied. On the fourth day of a low diet, blood samples were obtained for plasma renin activity (PRA) at 8:00 A.M., 11:00 A.M. and 5:00 P.M. On the same day a 24 hour urinary collection was obtained for the determination of aldosterone excretion. The following day 60 mg. of furosemide were given orally at 8:00 A.M. and another blood sample was drawn at noon. This study protocol was done before and after surgical correction of the aortic lesion. Mean systolic and diastolic blood pressure decreased significantly (P less than 0.005), while mean PRA and urinary aldosterone values showed no significant modifications after surgery. With these results, it is concluded that the renin-angiotensin-aldosterone system, does not seem to play a role in the chronic hypertension of the coarctation of the aorta. However, tests with angiotensin II specific blockers have to be performed before a definite conclusion can be drawn on this point.

Adolescent↗
PubMedDate not supplied

[Effect of alpha, beta blocker, labetol on the angiotensin renin system in arterial hypertension].

The effect of labetalol, a new alpha and beta adrenergic blocker, on blood pressure, heart rate, plasma renin activity (PRA), and urinary aldosterone excretion was assessed in 23 essential hypertensive patients, divided in 2 subgroups: 11 with normal electrocardiogram and 12 with left ventricular hypertrophy (LVH). In the first subgroup significant differences were found in the arithmethyc mean for sistolic blood pressure in sitting position (control: 166.1 +/- 17.2 mm of Hg treatment: 153.9 +/- 13.8, p less than or equal to 0.005) and in standing position (control: 165.3 +/- 17.3, treatment: 152.8 +/- 13.8, p less than or equal to 0.005) and for diastolic blood pressure (control: 102.7 +/- 12.6 to 89.9 +/- 10.1, p less than or equal to 0.001 and 103.2 +/- 11.8 to 91.2 +/- 10.8, p less than or equal to 0.001; in sitting and orthostatic positions, respectively.). No significant differences were found in the group with LVH. Heart rate decreased in the total population during treatment (- 6.0 +/- 7.5, p less than or equal to 0.05 and - 5.4 +/- 7.5 beats per minute, p less than or equal to 0.05 in sitting and orthostatic positions, respectively. PRA diminished in 12 of 15 cases studied (- 2.5 +/- 4.65 ng/ml/hr., p greater than 0.5). Correlation coefficient between decrements of diastolic blood pressure (sitting position) and ARP was 0.637. Aldosterone decreased in a non significant way during treatment. These data support the thesis of an important role of the adrenergic system in the pathogenesis of non complicated essential hypertension and, therefore, simultaneous alpha and beta receptor blockade in these cases has a better therapeutic effect. The good correlation between the decrements of ARP and blood pressure suggests an intervention of the inhibition of renin angiotensine system, brought about by the blocker property of labetalol, in the antihypertensive mechanism of the drug.

Angiotensin II↗
PubMedDate not supplied

[Arterial damage and the renin-angiotensin system in essential hypertension. Study of 63 cases].

Brunner, Laragh et al. have suggested that essential hypertensives with low plasma renin activity (PRA) are at lower risk of myocardial infarction or cerebrovascular accidents than those with high or normal PRA levels. In this paper we report on 63 patients with essential hypertension in whom the relation between PRA and the ocurrence of cardiovascular events was studied. The patients were categorized in high (11%), normal (70%) or low (19%) PRA subgroups, according to their 24-hour sodium excretion. Coronary angiogram was performed in 24 subjects. The three subgroups showed no significant differences in diastolic blood pressure, serum cholesterol levels, smoking habits or obesity. The incidence of cardiovascular complications was similar in patients with high or low PRA levels (28.5% and 33.3% respectively). In those hypertensives in whom coronary angiogram was done, coronary lesions were observed in 80% of the low renin subjects and in 37.5% of those patients with normal PRA. Therefore, no relation between PRA levels and vascular complications was observed in this series of patients. It is conclude that patients with essential hypertension must be treated as soon and effectively as possible regardless of their PRA value.

Adult↗
PubMedDate not supplied

[Aldosteronism after hypokalemia in diuretic therapy of systemic arterial hypertension].

Twenty-two cases with essential arterial hypertension were studied in the final part of a chronic period of treatment with Chlortalidona and in the first 30 days after treatment. Measurements of the following parameters were made: 1) Change in the excretion of urinary aldosterone (aldo). 2) Change in the arterial pressure (delta P). 3) Transtherapeutic serum potassium (delta K). 4) Change in the Q-T (delta QT) in the electrocardiogram. The measurements were made 3 days after the suppression of the drug and afterwards every 3 to 6 days for a month. The correlation of the K and QT was significant (r = 0.63). The P did not correlate with the K nor with the aldo (r = 0.14). The aldo was -5.92 +/- 3.1 ug./24 hs (p = 0.01) in those cases responsive to the drug. The disappearance of the antihypertensive effect occurred at 9.61 +/- 3.7 days and correlated with the normalization of the QT (r = 0.83) and the serum potassium. The delta aldo correlated with K (r = 0.56) and normalized 6.7 days after the suspension of the drug. The secondary aldosteronism participates in the parogenia of the transtherapeutic hypokalemia although with a slightly significant correlation. The important correlation between the disappearances of the antihypertensive effects and the electrocardiographic signs of hypokalemia may dwell in changes which directly or indirectly exercise the diuretic in the intracellular metabolism of K without necessarily cousing an antihypertensive effect additive of the same hypokalemia.

Adult↗
PubMedDate not supplied

[The renin-angiotensin-aldosterone system in the diagnosis of renovascular arterial hypertension].

Twenty one subjects with sistemic arterial hypertension and arteriographic signs of obstructive lesion of the renal artery were studied and classified in 3 groups: group A, 13 cases with bilateral renovascular lesions; group B, 4 patients with unilateral renovascular stenosis and group C, formed by 4 subjects with a segmental branch stenosis of a renal artery. In all cases an special protocol was followed to measure plasma renin activity (PRA) in blood taken from a peripheral vein, inferior vena cava and both renal veins and also to determine 24 hrs. urinary excretion of aldosterone (UEA). PRA and UEA were clasified as high, normal and low by comparing the results with those of normal subjects in a nomogram estimated in the same laboratory in which PRA and UEA values were correlated with 24 hrs. urinari sodium excretion. Besides, R greater than /R less than index (highest PRA of renal vein blood/PRA of contralateral renal vein) and V-A A index (V = PRA of renal vein blood; A = PRA of inferior vena cava) were calculated. Forty eight and thirty eight percentage of the cases had either high renin in peripheral venous blood or high UEA. Similar data in patients with essential hypertension previously studied in the same laboratory were 12 and 10% respectively. V-A A index was incongruent with the arteriographic image in 3 cases of group B; 4 cases of group A and 2 of group B had a pattern of bilateral stenosis, and one case in each group A and C had a unilateral stenosis pattern. In the other patients the samples were "non representative" due to a high level of PRA in the inferior vena cava blood comparable to PRA of the renal veins. Six cases of group A had a R greater than /R less than index superior to 1.5, which suggested a predominant vascular lesion in one side not always congruent with the arteriographic findings. In 3 cases of group B this index was higher than 1.5 in favor of the ipsilateral lesion. Three cases of group C had a normal R greater than /R less than index and one with a total oclussion of a segmental artery presented an index superior to 1.5, ipsilateral to the lesion. The latter index was of value in the diagnosis of renovascular arterial hypertension.

Aldosterone↗