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Biomedical subjects

G Valdés

Publications and source records attributed to G Valdés.

At least 19 recordsLinked to original sources
PubMed2005

Distribution of angiotensin-(1-7) and ACE2 in human placentas of normal and pathological pregnancies.

This work was designed to study the expression of the vasodilator peptide angiotensin-(1-7) [Ang-(1-7)] and its generating enzyme (ACE2) in the uteroplacental interface. Placentas were obtained from 11 early pregnancy failures (5 miscarriages and 6 ectopic pregnancies), 15 normotensive, and 10 preeclamptic gestations. In placental villi, the main sites of immunocytochemical expression of Ang-(1-7) and ACE2 were the syncytiotrophoblast, cytotrophoblast, endothelium and vascular smooth muscle of primary and secondary villi. Syncitial Ang-(1-7) expression in samples obtained from miscarriages and ectopic pregnancies was increased compared to normal term pregnancy [2.0 (2.0-2.25 for the 25 and 75% interquartile range) vs 1.3 (1.0-1.9), p<0.01]. In the maternal stroma, Ang-(1-7) and ACE2 were expressed in the invading and intravascular trophoblast and in decidual cells in all 3 groups. Ang-(1-7) and ACE2 staining was also found in arterial and venous endothelium and smooth muscle of the umbilical cord. The expression of Ang-(1-7) and ACE2 was similar in samples obtained from normal term or preeclamptic pregnancies, except for increased expression of ACE2 in umbilical arterial endothelium in preeclampsia [0.5 (0.5-0.8) vs 0.0 (0.0-0.0), p<0.01]. The uteroplacental location of Ang-(1-7) and ACE2 in pregnancy suggests an autocrine function of Ang-(1-7) in the vasoactive regulation that characterizes placentation and established pregnancy.

Angiotensin I↗
PubMed2001

Temporospatial changes of kinin b2 receptors during the estrous cycle and pregnancy in the rat uterus.

Tissue kallikreins are present in rat uterus during the estrous cycle in luminal and glandular epithelium, in early gestation in the implantation node, and in the last third of pregnancy surrounding the sinusoids in the decidua basalis. The pattern of kinin B2 receptor expression, through which the vasoactive effect of kallikreins is exerted, was studied by in vitro autoradiography and immunohistochemistry. The kinin B2 receptor was observed in the luminal and glandular epithelium, myometrium, endothelial cells of arteries, veins and venules, and smooth muscle cells of endometrial and myometrial arterioles. Immunoblotting of crude membranes revealed a band of 69 kDa that increased in late proestrus and estrus, concordantly with the pattern of immunostaining observed in the tissue. At Day 7 of gestation, the kinin B2 receptor was expressed (binding sites and receptor protein) in the epithelium of the implantation node and decidual cells; these latter cells showed a further increase during gestational Days 9 and 10. From Days 14 to 21, the subplacental decidua became strongly immunoreactive, and on Days 16 and 21 the placental labyrinthine endothelium was intensely stained. During this period, endothelium of arteries and veins, smooth muscular cells of small diameter arterioles, and myometrium also expressed B2 receptors. In unilaterally oil-stimulated pseudopregnancy, the decidual cells and the glandular epithelium show similar immunoreactivity to that during pregnancy. The temporospatial pattern of kinin B2 receptors, coinciding with that of kallikrein or with sites accessible to the generated kinins, further supports an autocrine-paracrine role for the kallikrein-kinin system in the vasoactive changes of implantation and placental blood flow regulation.

Animals↗
PubMed2001

Tissue kallikrein in human placenta in early and late gestation.

This study was addressed to identify kallikrein mRNA and protein in early, preterm, and term human placenta and to evaluate their temporospatial pattern. Kallikrein mRNA was expressed in syncytio/cytotrophoblasts and in the endothelial cells of the floating villi, with a greater intensity in early samples (isolated spontaneous abortions and ectopic pregnancies). Cytotrophoblasts at the base of the anchoring villi, maternal decidua and decidual arteries, endothelial cells of chorionic and basal plate blood vessels, and the amniotic epithelium presented a positive signal. Tissue kallikrein was predominantly observed in syncytiotrophoblasts and had a greater immunoreactivity in first-trimester samples. Intraarterial trophoblasts, blood vessels of the floating villi, basal and chorionic plates, and the amniotic epithelium showed positive immunoreactivity. The sites and variations of the tissue kallikrein mRNA and protein in the human placenta, in different stages of pregnancy, support the hypothesis that this enzyme may participate in the establishment and maintenance of placental blood flow through vasodilation, platelet antiaggregation, cell proliferation, and trophoblast invasion.

Abortion, Spontaneous↗
PubMed2001

Urinary vasodilator and vasoconstrictor angiotensins during menstrual cycle, pregnancy, and lactation.

Since normal human pregnancy is characterized by normotension in the face of an increased renin-angiotensin-aldosterone system (RAAS), we evaluated the temporal pattern of urinary excretion of a novel vasodilator within this system, angiotensin-(1-7) (Ang-[1-7]), during the menstrual cycle, pregnancy, and lactation. The urinary profiles of Ang I, Ang II, human chorionic gonadotropin, 17beta-estradiol, and progesterone were also determined. During the menstrual cycle, urinary Ang-(1-7) and Ang II remained stable (mean cycle value: 94.6 +/- 11.3 and 11.4 +/- 1.1 pmol/g of creatinine, respectively) in nine females. In 10 normal pregnant women, urinary Ang-(1-7) and Ang II increased throughout gestation, averaging 1499.8 +/- 310 and 224.4 +/- 58 pmol/g of creatinine, respectively (p < 0.05) at wk 35 and falling during lactation to 394.0 +/- 95 and 65.7 +/- 20 pmol/ g of creatinine (p < 0.05), respectively. The Ang-(1-7)/Ang II ratio was unchanged in the different reproductive periods. During the menstrual cycle, Ang II and Ang-(1-7) correlated with 17beta-estradiol and progesterone using multivariate analysis (r = 0.31, p < 0.001) and r = 0.28, p < 0.02, respectively). During gestation, 17beta-estradiol and progesterone correlated with urinary Ang-(1-7) (r = 0.48, p < 0.001 and r = 0.47, p < 0.001, respectively) and Ang II (r = 0.24, p < 0.03 and r = 0.25, p < 0.03, respectively); by multiple regression, only Ang-(1-7) correlated with both steroids (r = 0.49,p < 0.001). The progressive rise of Ang-(1-7) throughout gestation, probably modulated by estrogen and progesterone, suggests a physiologic counterregulation within the RAAS.

Adult↗
PubMed2001

Tissue kallikrein and bradykinin B2 receptor in human uterus in luteal phase and in early and late gestation.

This study was addressed to evaluate the temporospatial pattern of key components of the kallikreinkinin system in human uterus in luteal phase (n = 7), early pregnancy (isolated spontaneous abortions, n = 11; ectopic pregnancies, n = 9), idiopathic preterm deliveries (n = 5), and term gestations (n = 12). Tissue kallikrein mRNA and protein and the type 2 bradykinin receptor (B2R) protein were expressed in luminal and glandular epithelium and in endothelial cells of stromal and myometrial blood vessels, while tissue kallikrein mRNA and B2R, but not tissue kallikrein protein, were observed in decidual cells and in arteriolar and myometrial muscle. A greater signal intensity for tissue kallikrein mRNA and protein and of B2R protein was observed in the early pregnancy samples. The sites and variations of the tissue kallikrein mRNA and protein and of the B2R protein in the human uterus and in fallopian tubes during the luteal phase and in pregnancy coincide with those described for other vasoactive effectors such as nitric oxide, prostacyclins, growth factors, and renin. The uterine localization of the main enzyme and receptor of the tissue kallikrein-kinin system in key sites for embryo attachment, implantation, placentation, maintenance of placental blood flow, and parturition supports the notion that the kallikreinkinin system participates in these processes, probably through vasodilation, increased vasopermeability, enhanced matrix degradation, stimulation of cell proliferation, and myometrial contractility.

Adult↗
PubMed2001

[Refractory arterial hypertension and the use of anticonvulsant drugs. Case report].

Resistant arterial hypertension is uncommon when there is good compliance to antihypertensive therapy and secondary causes have been ruled out. We report a 41 years old male that suffered hypertensive encephalopathy and received prophylactic anticonvulsant therapy showing progressive raise of arterial pressure levels. Renovascular hypertension, aldosteronism and pheochromocytoma were discarded and, in spite of combined use of antihypertensive drugs, he did not achieve normal blood pressure. When phenytoin was discontinued, blood pressure temporarily normalized. Carbamazepine was started and blood pressure raised again. It fell when this medication was discontinued. Antiepileptic agents could induce drug metabolizing system and thus reduce the effects of antihypertensive medications.

Adult↗
PubMed2000

[Endothelial dysfunction as a primary disorder in vascular diseases].

Endothelium controls vascular smooth muscle tone by secreting relaxing and contracting factors. There is a constant release of endothelium derived relaxing factors, mainly nitric oxide, a potent vasodilator, inhibitor of platelet aggregation, monocyte adhesion and smooth muscle proliferation. In addition, the endothelium may increase the release of NO in response to humoral stimulation by vasoactive substances such as acetylcholine, bradykinin or substance P. Although the endothelium releases a number of products, no single blood test has yet proved useful to determine normal endothelial function or as early abnormalities. The most useful test of endothelial function relies on the measurement of endothelium-dependent dilatation in response to pharmacological or physiologic stimuli. The alteration of this response is known as endothelial dysfunction and has been observed in a variety of circumstances related to cardiovascular risk. This review summarizes the evidence that sustains this association and emphasizes the clinical utility of assessing endothelial function presenting two clinical cases of hypercholesterolemia in which a high-resolution vascular ultrasound in the brachial artery was used.

Adult↗
PubMed1999

[Recommendations for the use of ambulatory blood pressure monitoring. Consensus document of the Chilean Hypertension Society].

Continuous ambulatory blood pressure monitoring is a diagnostic technique devised as a consequence of the great variations in blood pressure measurements. It allows multiple daily measurements, nocturnal monitoring, avoids the stress of blood pressure measurements, gives a picture of pressure behavior during 24 hours and reduces observer related errors. The equipment used must be accurate and validated using international protocols. Accepted indications for continuous ambulatory blood pressure monitoring are white coat hypertension, episodic hypertension, resistance to medications and assessment of symptoms or autonomic dysfunction. Other indications with less clear cut usefulness, are high risk cardiac, renal or pregnant patients and an accurate blood pressure control. We describe equipment calibration, elements that must be considered in the reports, result interpretation and conclusions. Normal blood pressure ranges for children and pregnant women are also reported.

Age Factors↗
PubMed1998

[Measurement of low levels of plasma renin activity. A methodological improvement].

BACKGROUND: The present method to measure plasma renin activity is cumbersome and imprecise, factors that limit its clinical application. AIM: To assess the importance of blood sampling conditions and the usefulness of increasing incubation time to measure plasma renin activity at low levels. PATIENTS AND METHODS: Twenty hypertensive patients, 14 female, aged 14 to 76 years old, were studied. Two blood samples were obtained after a 10 min rest in the sitting position and after a 30 min rest in supine position. One blood sample of each condition was sent to the laboratory at room temperature and the other sample was sent refrigerated. Angiotensin I concentration was determined after 3 h of enzymatic incubation at 37 degrees C and, in subjects with an activity of less than 1 ng/ml/h, after 18 h of incubation. RESULTS: No significant differences in plasma renin activity were observed between the samples obtained with different rest times or different transportation methods. In people with low plasma renin activity, the 18 h enzymatic incubation reduced the lower detection from 0.3 to 0.014 ng/ml/h and the coefficient of variation from 14.4 to 3.2%. CONCLUSIONS: A simplified blood sampling method does not change plasma renin activity values, and the longer enzymatic incubation in people with low plasma renin activity improves both the sensitivity and accuracy of the determination.

Adolescent↗
PubMed1998

The kallikrein-kinin system along the different stages of gestation: experimental and clinical findings.

We analyse the data accumulated on the description of the uterine kallikrein-kinin system in estrous cycle, pregnancy, pseudopregnancy and hormonal supplementation, and discuss the possible role of these findings in relationship to the vasoactive changes of gestation. We conclude that the evidence supports a participation of kallikrein in implantation and maintenance of uteroplacental blood flow. A decreased urinary kallikrein in women in conditions of an impaired uterine blood flow might be related to a deficient response of this vasodilator system.

Animals↗
PubMed1997

Estrogen and luminal stimulation of rat uterine kallikrein.

To understand the regulation of rat uterine kallikrein, we evaluated its variations in animals that had been ovariectomized and supplemented with estradiol or progesterone, in pseudopregnant animals intraluminally oil-stimulated or unstimulated, and in unilaterally pregnant animals. The content of kallikrein, determined by an RIA highly specific for rK1 (true tissue kallikrein), rose in ovariectomized rats with estradiol supplementation (0.28 +/- 0.03 to 0.44 +/- 0.05 ng/mg) and decreased with progesterone (0.13 +/- 0.02 ng/mg; n = 15; p < 0.001). Kallikrein content rose from Day 1 of pseudopregnancy (PP1) to a maximum on PP7 (0.18 +/- 0.01 to 0.39 +/- 0.04 ng/mg protein; n = 36; p < 0.001). On PP7 with unilateral oil intraluminal stimulation, the decidualized horn had higher kallikrein content than did the contralateral (0.98 +/- 0.09 vs. 0.35 +/- 0.05 ng/mg protein; n = 7; p < 0.001). Immunocytochemistry revealed that mainly rK1 is localized in the luminal and glandular epithelium, and it increased in the stimulated horn. In the unilaterally pregnant rat on Day 7, the fertile horn had a higher kallikrein content than its contralateral control (0.71 +/- 0.07 vs. 0.37 +/- 0.03 ng/mg protein, p < 0.001; n = 8), as well as a higher kininogenase activity (239 +/- 34.3 vs. 83.5 +/- 7.9 ng bradykinin(BK)/h per horn, p < 0.003; and 945 +/- 90 vs. 585 +/- 40 ng BK/h per gram tissue, p < 0.002; n = 6). These results indicate that estrogen stimulates, whereas progesterone inhibits, kallikrein production, and that hormonal regulation is overridden by intraluminal stimulation, thus associating the enzyme with decidualization.

Animals↗
PubMed1996

Temporospatial changes of kallikrein-like enzymes during the estrous cycle and pregnancy in the rat uterus.

We have recently reported the presence of uterine glandular kallikrein in the rat, its mRNA, and its increase in early gestation. This study describes its immunolocalization, by polyclonal antibodies against rat urinary kallikrein, during the estrous cycle and pregnancy, and identifies three members of the kallikrein family. During the estrous cycle, immunoreactivity, represented by an apical rim in the luminal and glandular epithelium, was greater during proestrus. On Day 5 of gestation, the reaction increased, and on Day 6 staining appeared in the apical and basal pole of some cells. On Day 7, staining was markedly increased in the glandular epithelium at the implantation site, frequently occupying the whole cytoplasm, and displaying great intensity in isolated glandular cells; the epithelium of the implantation chamber showed apical immunoreactivity, while the interimplantation zone had a few faintly stained glands. At this stage, the staining represented expression of two of the enzymes, rK1 and rK7. On Days 9 and 10, the staining disappeared, to reappear on Day 12 in the cells underlying the blood vessels of the central subplacental region. On Days 16 and 21, kallikrein staining surrounded the subendothelium of the sinusoids of the whole decidua basalis. This subplacental reaction represented expression of rK1, rK2, and rK7. This study shows important changes in the immunocytochemical expression of three uterine kallikrein-like enzymes during the reproductive cycle, associated with different hormonal milieus and with local stimulation. The localization of these enzymes is associated with areas involved in implantation, trophoblast penetration, and placental blood flow regulation.

Animals↗
PubMed1994

Variations in uterine kallikrein during cycle and early pregnancy in the rat.

We have previously demonstrated the presence of tissue kallikrein and its mRNA in rat uterus, and an increase of the immunoreactive enzyme on Day 7 of gestation, which suggests a hormonal regulation and a role in implantation. This study pursued the sequential variations during the cycle and early pregnancy. During the estrous cycle, immunoreactive uterine kallikrein levels showed a recurrent pattern, with the highest value on proestrus (12.9 +/- 1.5 ng/uterus or 0.49 +/- 0.03 ng/mg protein), and the lowest on metestrus (4.1 ng +/- 0.5 ng or 0.30 +/- 0.03 ng/mg protein); p < 0.05. During gestation, values on Day 1 (6.1 +/- 0.4 ng/uterus or 0.30 +/- 0.01 ng/mg protein) and Day 3 (4.9 +/- 0.3 ng or 0.35 +/- 0.01 ng/mg protein) were similar to levels during estrus and diestrus; a progressive rise, observed from Day 5 (8.2 +/- 1.1 ng or 0.43 +/- 0.02 ng/mg protein), attained the highest value on Day 7 (15.8 +/- 1.7 ng or 0.78 +/- 0.05 ng/mg protein); p < 0.05. The variations observed during the cycle and early gestation coincide with those described for ovarian steroids and uterine vasoactive changes, suggest the hormonal regulation of uterine kallikrein levels, and support its role in implantation.

Animals↗
PubMed1993

Uterine kallikrein in the early pregnant rat.

Uterine homogenates of cycling and early pregnant Sprague Dawley rats and purified rat urinary kallikrein showed similar curves of displacement of 125I-kallikrein binding to a polyclonal antibody. Uterine kallikrein concentration measured by RIA was 8.7 +/- 2 SEM ng/g wet weight during the cycle (n = 6 in diestrus and metestrus) and 20.8 +/- 2 SEM (n = 7) ng/g wet weight on Day 7 of pregnancy (P7) (p < 0.001). On P7, kallikrein concentration was increased 12.4-fold in the implantation nodes, as compared to the interimplantation segments. Uterine homogenates of rats on P7, submitted to DEAE-cellulose chromatography and Sephadex gel filtration, yielded two fractions containing kallikrein immunoreactivity and kininogenase activity, with molecular masses that ranged from 120-125 kDa and 39-43 kDa, respectively. In the RIA, both fractions displayed parallelism with purified kallikrein. Enzymatic activity was expressed after activation by trypsin. It was inhibited by aprotinin, PMSF, p-amino-benzamidine, and leupeptin, but not by soybean or ovomucoid trypsin inhibitors. Kallikrein mRNA was demonstrated by reverse transcriptase/polymerase chain reaction in uteri of nonpregnant and P7 rats. These results show that rat uterus synthesizes one or more serine proteases that are immunologically and enzymatically related to tissue kallikrein in the implantation node on P7--determined both by an increment of whole uterus kallikrein content and a depletion of the interimplantation segments--suggests that kallikrein may play a role in the vasoactive changes of implantation.

Animals↗
PubMed1993

[Kidney transplantation and pregnancy: experience with 6 patients].

From 1983 to 1991, six pregnant women bearing a renal transplant were admitted at the P Universidad Católica de Chile Clinic Hospital. All of them were under immunosuppressive therapy with azathioprine and prednisone. One patient was also receiving cyclosporine. Four had chronic hypertension; 1 presented intrahepatic cholestasis of pregnancy; 2, premature rupture of membranes, and 3, preeclampsia (superimposed to chronic hypertension). There were no abortions. The median gestational age at delivery was 35.5 weeks. Only one of the six newborns was small for gestational age; the others were of appropriate size. There were no neonatal problems or congenital anomalies. Deterioration of the renal function was observed in two patients. One patient presented rejection to the transplanted kidney. Pregnancy following renal transplantation is not exempt of risks, but multidisciplinary management, close prenatal control and opportune interruption of gestation play a key role in the successful outcome of these pregnancies.

Adult↗
PubMed1993

[Treatment of mild hypertension with captopril and captopril with hydrochlorothiazide. Impact on blood pressure values and quality of life].

The effects of captopril alone or associated to hydrochlorothiazide on blood pressure and quality of life was studied in 244 hypertensive subjects. After a medication wash out period of 30 days (and 7 additional days when diuretics were used) patients were treated initially with captopril 25 mg b.i.d. (scheme A); if blood pressure was not normalized, hydrochlorothiazide 25 mg o.d. was added (scheme B) and the dose of captopril was increased to 50 mg bid (scheme C) in a stepwise fashion. Sixteen patients (6.6%) were lost from follow up; in the rest a significant reduction of blood pressure was obtained at the end of the treatment period (from 163/98.9 +/- 19.7/3.1 to 143/85 +/- 12.7/6.7 p < 0.05), without changes in cardiac frequency. Using captopril alone, blood pressure was normalized at 15 and 75 days in 62.9 and 70.6% of patients respectively. With captopril plus hydrochlorothiazide blood pressure was normalized in 80.9% of patients. Quality of life improved significantly from of 42.8 +/- 1.7 to 50.7 +/- 15 score points (p < 0.05) secondary effects were observed in 7.4% of patients. It is concluded that captopril alone or associated to hydrochlorothiazide is effective in the treatment of mild hypertension, produces few secondary effects and improves the quality of life.

Adult↗
PubMed1993

[Renal scintigraphy with captopril in the evaluation of renovascular hypertension].

The administration of an angiotensin-converting enzyme (ACE) inhibitor transitorily reduces the GFR in a kidney with renal artery stenosis, effect that can be ascertained with scintigraphic studies using ACE inhibitors. We evaluated the clinical usefulness of captopril renography (CR) in the diagnosis of renovascular hypertension (RVH) in 51 hypertensive patients in which this diagnosis was suspected. All subjects underwent angiography and RVH was diagnosed when renal artery stenosis exceeded 60%, there was lateralization of renal vein renin or there was a concordant clinical outcome. Renography was performed 15 minutes after Lasix administration, using Tc-99m DTPA, before and 60 minutes after the oral administration of 50 mg of captopril. The scintigraphic criteria for a positive test were a decreased split renal function, a delayed peak uptake, a decreased excretion of DTPA and a prolonged transit time. In three of 28 patients in whom angiography discarded RVH, CR was positive. In the 23 patients with confirmed RVH, CR was positive in 10 of 12 with unilateral stenosis, in 3 of 8 with bilateral stenosis and 1 of 3 with stenosis in a transplanted kidney. The overall sensitivity and specificity of the test for RVH was 60.9% and 89.2% respectively. There were no changes in blood pressure or adverse effects after captopril administration. We conclude that CR in RVH is useful to select patients for further studies (angiography) and to perform a functional interpretation of angiographic alterations.

Adolescent↗