Biomedical subjects

A Damasceno

Publications and source records attributed to A Damasceno.

10 recordsLinked to original sources

PubMed2000

Renal dopaminergic mechanisms in renal parenchymal diseases, hypertension, and heart failure.

The recovery of renal function in renal transplant recipients is accompanied by an enhanced ability to synthesize dopamine (DA), which may contribute to maintain sodium homeostasis. Patients suffering from chronic renal parenchymal disease, a well-recognized form of salt sensitive (SS) hypertension, have a reduced ability to produce DA that correlates well with deterioration of renal function. In patients afflicted with IgA nephropathy, but normal renal function, urinary excretion of DA correlated positively with BP responses to changes from 200 to 20 mmol/day salt intake. In black salt resistant (SR) normotensives (NT) and SR hypertensives, under low salt intake (40 mmol/day), but not SS-NT and SS-HT, the saline infusion induced increments of DA and DOPAC urinary excretion correlated significantly with increments of sodium urinary excretion and sodium fractional excretion. Patients afflicted with heart failure (HF) have a reduced delivery of L-DOPA to the kidney, accompanied by an increase in DA/L-DOPA urinary ratios. This suggests that HF patients have an increased ability to take up or decarboxylate L-DOPA. Sodium restriction resulted in a significant decrease in urinary L-DOPA, DA and DOPAC in HF patients, suggesting that the system responds to sodium. It is concluded that activity of renal dopaminergic system may be altered in SS subjects, despite the level of their BP, and an enhanced delivery of L-DOPA to the kidney may be beneficial in edema formation states.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2000

Influence of salt intake on the daytime-nighttime blood pressure variation in normotensive and hypertensive black subjects.

OBJECTIVE: To evaluate the influence of different salt-intake regimens on the circadian rhythm of blood pressure (daytime-night-time relationship) in normotensive and hypertensive black subjects with different patterns of salt sensitivity. METHODS: Randomized, cross-over study. Twenty normotensive (NT) and 27 hypertensive (HT) black subjects were kept on a low-sodium diet (30 mmol sodium/d, LS) and on a high-sodium diet (300 mmol sodium/d, HS) for 1 week each. On the last day of each regimen, 24 hour ambulatory blood pressure monitoring was performed. RESULTS: Eight normotensives were classified as salt-sensitive (SS), all with haptoglobin phenotypes (FeHap) 1,1 or 1,2, and 12 as salt resistant (SR), 5 with FeHap 2,2. Seventeen hypertensives were classified as SS, all with FeHap 1,1 or 1,2, and 11 as SR, 2 with FeHap 2,2. Salt sensitivity criterium was: difference > 5 mmHg of 24 h mean blood pressure from low sodium to high sodium. The pattern of daytime-nighttime blood pressure relationship between LS and HS was only modified (respectively from dipper to non-dipper) in HT-SS, but not in NT-SS, NT-SR and HT-SR. The percentual drop in nighttime mean blood pressure was about 10% in HT-SR and in NT-SR either under LS or HS. In NT-SS, the percentual night-time drop in mean blood pressure was lower than that of NT-RS (i.e. about 7-8%), but it was not different on LS and on HS. In contrast, in HT-SS, the percentual nighttime drop in mean blood pressure on HS (6%) was significantly lower than that on LS (10%, p < 0.01). In the 27 HT, but not in the NT, changes in the nocturnal drop in mean blood pressure induced by salt restriction correlated positively with the degree of salt sensitivity (r = 0.45, p < 0.05). CONCLUSIONS: In black subjects, the pattern of nighttime-daytime blood pressure relationship appears to be modified from LS to HS diets (or vice-versa) only in SS hypertensive subjects, but neither in NT-SS nor in NT-SS and HT-SR. Only in HT-SS, but not in the other groups, salt restriction shifts the circadian rhythm of blood pressure from a non-dipper to a dipper pattern. We conclude that in black salt-sensitive hypertensives, salt restriction improves the circadian rhythm of blood pressure. This may have important therapeutic consequences on target organ damage associated with non-dipper patterns.

Adult↗

PubMed1999

Deficiency of renal dopaminergic-dependent natriuretic response to acute sodium load in black salt-sensitive subjects in contrast to salt-resistant subjects.

OBJECTIVE: To evaluate the involvement of the renal dopaminergic system in the natriuretic responses to acute saline load in salt-resistant (SR) and salt-sensitive (SS) black normotensive (NT) and hypertensive (HT) subjects. DESIGN AND METHODS: We studied the relationship between the urinary excretion of dopa, dopamine (DA) and its metabolite DOPAC and the natriuretic responses to acute volume expansion (2 l NaCl 0.9% over 2 h) in 20 black NT subjects (12 SR and 8 SS) and 19 black HT subjects (10 SS and 9 SR). Subjects received a low salt (LS) diet (40 mmol sodium/day) for 1 week and a high salt (HS) diet (300 mmol sodium/day) for 1 week; the sequence of the dietary regimens was randomized. Comparisons were made between the results before the saline infusion (baseline) and the results 2 h after the infusion. RESULTS: In all the groups saline infusion induced significant increases in urinary volume (ml/4 h) of two- to three-fold and in urinary sodium excretion (mmol/4 h) of three- to ten-fold; these increases were significantly greater during the HS diet than during the LS diet. Saline infusion significantly increased the mean arterial pressure (MAP) by 5 mmHg in HT-SS subjects and by 4-5 mmHg in NT-SS subjects, but the MAP did not changed in the NT-SR and HT-SR groups. Under the LS diet, saline infusion changed the DA excretion (in nmol/4 h) by -49+/-89 in HT-SS subjects, by 17+/-52 in NT-SS subjects, by 235+/-72 in HT-SR subjects and by 220+/-86 in NT-SR subjects (P < 0.05 between SR and SS subjects). The saline infusion-induced changes in DA excretion correlated significantly with the increases in urinary sodium excretion (r = 0.71, P < 0.01) in the NT-SR and HT-SR subjects under the LS diet, but not in the SR groups on the HS diet nor in the SS groups (HT and NT) on either diet. Saline infusion significantly reduced the DA/dopa ratio in SS (NT and HT) but not SR (NT and HT) subjects, whereas the DA/DOPAC (dihydroxyphenylacetic acid) ratios were similar in all the groups. CONCLUSIONS: The urinary dopaminergic system may participate in the natriuretic responses to acute sodium load only in SR subjects (NT and HT) and only under LS diets, but not in SS subjects (NT and HT). This strongly suggests that black NT- and HT-SS subjects have an underlying impairment in the activity of the renal dopaminergic system which may be associated with a reduced decarboxylation of dopa into DA.

Adult↗

PubMed1999

Acute hypotensive, natriuretic, and hormonal effects of nifedipine in salt-sensitive and salt-resistant black normotensive and hypertensive subjects.

In a randomized double-blind study, we compared the short-term effects of nifedipine (10 mg 3x daily for 1 day) versus placebo on 24-h blood pressure, diuresis, natriuresis, urinary excretion of dopamine and metabolites, and on plasma renin activity (PRA) and plasma aldosterone levels in 18 black hypertensive (HT) patients [eight salt-resistant (HT-SR) and 10 salt-sensitive (HT-SS)], and in 20 black normotensive (NT) subjects (12 NT-SR and eight NT-SS) who were studied randomly with both a high- (HS) and a low-salt (LS) diet. In comparison to placebo, nifedipine significantly decreased 24-h mean BP in all groups either with HS or LS diets (all p<0.05). With HS, greater hypotensive effects were achieved in NT-SS (-10+/-2 mm Hg) versus NT-SR (-3+/-1 mm Hg; p<0.05) and in HT-SS (-18+/-2 mm Hg) versus HT-SR (-12+/-2 mm Hg; p<0.05). In NT-SS and HT-SS, nifedipine induced greater (p<0.05) BP decrease with HS (-10+/-2 and -18+/-2 mm Hg) than with LS (-4+/-1 and -9+/-1 mm Hg, respectively), whereas in NT-SR and HT-SR, the hypotensive effect did not differ between HS and LS. Nifedipine versus placebo significantly increased natriuresis and fractional excretion of sodium in all groups only with HS (p<0.05) but not with LS diets. Only in HT-SS were the hypotensive and natriuretic effects of nifedipine significantly correlated (r = -0.77; p<0.01). Nifedipine produced a similar increase of the urinary excretion of dopamine, L-DOPA, and of DOPAC in all subjects, which did not correlate with hypotensive and natriuretic effects. Nifedipine did not modify plasma levels of renin and of aldosterone except in NT-SS with HS, in whom nifedipine increased PRA levels (p <0.05). We conclude that although nifedipine reduces BP in all groups of NT and HT with LS and HS diets, the effect is greater in salt-sensitive subjects with HS. Although in HT-SS with HS, the short-term natriuretic response to nifedipine may contribute to its hypotensive effects, the diuretic-natriuretic effect of nifedipine is not necessary for the expression of its hypotensive effect. Moreover, it is unlikely that any short-term effects of nifedipine either on the renal dopaminergic system or on the secretion of aldosterone explain nifedipine short-term hypotensive and diuretic-natriuretic effects.

Adult↗

PubMed1999

[The additional efficacy of the nifedipine-diuretic combination depends on the potency of the drug administered first and not the sequence of administration. A double blind study in salt-sensitive black hypertensives].

OBJECTIVE: To evaluate whether the additional antihypertensive efficacy of the nifedipine-thiazide combination depends on the sequence of drug administration and whether the natriuretic effect of thiazide persists when co-administered with nifedipine. METHODS: Double blind, randomised, crossover, placebo-controlled study, in 12 salt-sensitive hypertensive black patients (SSH). Evaluation of the antihypertensive (24 h ambulatory monitoring) and natriuretic effects of placebo (PL), of nifedipine-GITS (NIF, 30 mg/d) and of hydrochlorothiazide (HCTZ, 25 mg/d) given alone and in combination within two separate therapeutic sequences: PL-->NIF-->NIF + HCTZ and PL-->HCTZ-->HCTZ + NIF (1 month for each therapeutic regimen). RESULTS: NIF induced greater (p < 0.04) reduction of 24 h mean arterial pressure (MAP) (-15.9 +/- 1.9 mm Hg, v PL) than HCTZ (-9.0 +/- 1.3 mm Hg). The association of NIF to HCTZ induced a greater (p < 0.05) additional reduction of MAP-24 h (9.7 +/- 2.2 mm Hg) than that produced by the association of HCTZ to NIF (4.1 +/- 1.3 mm Hg). NIF alone and in combination did not modify the diuresis-natriuresis observed with the previous treatment, whereas HCTZ alone and in combination always increased diuresis (by 25%) and natriuresis (by 53%). There was a significant negative correlation (r = -0.71, p < 0.001) between blood pressure (BP) reduction induced by the drug administered first (NIF or HCTZ) and the additional BP reduction obtained by the association of the second drug. CONCLUSIONS: In most of the SSH the NIF-GITS was more potent than HCTZ. NIF did not modify the diuretic-natriuretic effect of PL and of HCTZ. The greater potency of NIF may explain why in most patients the combination HCTZ to NIF induced a lower hypotensive effect than that of the association of NIF to HCTZ. Independently of the sequence of the drug administration, the lower the hypotensive effect of the drug administered first the greater the additional hypotensive effect that was observed by adding the second drug.

Adult↗

PubMed1998

Nifedipine-retard versus nifedipine-capsules for the therapy of hypertensive crisis in black patients.

In a randomized parallel-group placebo-controlled study, we compared the short-term hypotensive efficacy and the safety of a single administration of nifedipine-retard (20-mg tablets) with that of two administrations 6 h apart of nifedipine capsules (10 mg) in 10 and 11 black patients, respectively, with acute severe hypertension. Both groups had similar pretreatment blood-pressure (BP) values. Blood pressure was recorded at 10-min intervals for 12 h by using an automated device. In the first 3 h of treatment, nifedipine capsules induced a faster and greater hypotensive effect than nifedipine retard, which was associated with an increase in heart rate. At 2 h after treatment, nifedipine capsules decreased BP to levels (159 +/- 5/105 +/- 3 mm Hg) that were significantly lower than those reached by nifedipine-retard (175 +/- 4/118 +/- 4 mm Hg; p < 0.05). Both preparations induced a similar maximal BP decrease of approximately 30% of the placebo values, but the peak decrease of BP occurred significantly later with nifedipine-retard (283 +/- 31 min after administration) than with nifedipine capsules (100 +/- 14 min; p < 0.01). Four hours after administration, the hypotensive effect of nifedipine capsules was blunted, and a second administration was necessary, whereas nifedipine-retard reduced BP slowly and continuously for < or =12 h and more smoothly. Flush and headache were more frequently found with nifedipine capsules. We conclude that in black patients with hypertensive crisis, nifedipine capsules produce an abrupt decrease in BP that may be potentially harmful. Thus for patients suitable for treatment with nifedipine, nifedipine-retard is preferable because it effectively reduces BP for > or =12 h while achieving a rapid enough effect without critical short-term decreases in BP.

Administration, Oral↗

PubMed1997

Efficacy of captopril and nifedipine in black and white patients with hypertensive crisis.

We examined the antihypertensive efficacy of: (1) sublingual-oral single doses of captopril (25 mg) and nifedipine-capsules (10 mg) in 9 + 9 white patients and in 9 + 8 black patients with hypertensive crisis; and (2) a single oral dose of the slow-acting preparation of nifedipine-retard (20 mg) in another 10 black patients. Blood pressure (BP) was assessed at 10 min intervals for 6 h after administration. After 6 h, the BP falls induced by these drugs were still significantly lower than the baseline placebo values. Hypotensive effect of nifedipine-capsules was established more rapidly than that of captopril in both white and black patients, and of nifedipine-retard in black patients. Considering the area under the curve of BP values during the 6-h treatment, the overall hypotensive effect of nifedipine-capsules was similar to captopril in white patients, but significantly more pronounced than captopril and nifedipine-retard in black patients. In white patients similar maximal drops of BP (mean+/-s.e.m.) were obtained with nifedipine-capsules (71+/-4/52+/-4 mm Hg) and with captopril (69+/-4/50+/-3 mm Hg). In black patients the maximal drop of BP of nifedipine-capsules (70+/-4/52+/-4 mm Hg) was greater (P < 0.02) than that of captopril (48+/-4/32+/-3 mm Hg) but similar to that of nifedipine-retard (71+/-4/49+/-4 mm Hg). However, in contrast to nifedipine-capsules and captopril, nifedipine-retard produced a slower drop in BP. The time of peak drop in BP of both nifedipine-capsules and captopril occurred within the first 2 h whereas with nifedipine-retard it occurred only between 4 and 6 h after administration. Fewer patients reported side effects with nifedipine-retard as compared with the other two preparations. We conclude that single doses of captopril and nifedipine reduces BP for at least 6 h in both white and black patients with hypertensive crisis, but nifedipine is more potent than captopril in black patients. The slow release form of nifedipine-retard effectively and safely lowers BP while achieving a rapid enough effect without the critical rapid falls in BP that occur with nifedipine-capsules.

Administration, Oral↗

PubMed1993

[Mitral subvalvular aneurysm: report of 3 cases].

Mitral annular subvalvar Aneurysms are a very uncommon pathology and almost restricted to Blacks Africans. The authors present three cases, describing their clinical presentation, evolution and complications. The complementary exams are also presented and their relevance in the diagnosis is discussed.

Adult↗

PubMed1993

[Mitral subvalvular aneurysm].

Mitral subvalvar aneurysms are a rare clinical entity and not commonly described in the literature. They are almost exclusive of the black population in the subsaharian Africa. The authors, in a bibliographic revision, present the different etiological theories, the pathology, the pathophysiology, the clinical presentation and discuss the relative value of the different diagnostic tools. The differential diagnosis is also discussed and the more recent methods of medical and surgical treatment presented.

Coronary Angiography↗

PubMed1992

[Two cases of endomyocardial fibrosis in Mozambique].

This essay describes two cases of Endomiocardial Fibrosis with right ventricular dominance studied in Mozambique. The clinical, radiological, echocardiographic and patological findings are in accordance with other descriptions of same disease, seen in others countries.

Adolescent↗