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Javier Palacios

Publications and source records attributed to Javier Palacios.

5 recordsLinked to original sources

Na+ -K+ -2Cl- cotransporter is implicated in gender differences in the response of the rat aorta to phenylephrine.

Inhibition of the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) with bumetanide reduced contractile responses to phenylephrine (PE) in male rat aortas (129+/-4% of 60 mM KCl-induced contraction control vs 108+/-7% bumetanide; PE 10(-5) M; P<0.01) but did not change equivalent responses in female rat aortas. Removal of the endothelium blunted the effect of NKCC1 inhibition on the response to PE (10(-5) M) in males, whereas in denuded aorta from female rats, bumetanide reduced this response (162+/-5% control vs 146+/-3% bumetanide; P<0.05). NKCC1 basal activity did not show gender differences in intact aortic rings, but in the presence of PE, bumetanide-sensitive (86)Rb(+)/K(+) uptake increased more in male than female aortas (179+/-8 in males vs 158+/-5 nmol (86)Rb(+)/K(+) min(-1) (g aorta)(-1) in females; P<0.05). PE did not stimulate NKCC1 activity in denuded aorta from male rats. However, in female rats, PE increased NKCC1 activity similarly in both denuded (169+/-11 nmol (86)Rb(+)/K(+) min(-1) (g aorta)(-1)) and intact aortas. Ovariectomy increased the bumetanide-sensitive (86)Rb(+)/K(+) uptake increase elicited by PE (223+/-17 nmol (86)Rb(+)/K(+) min(-1) (g aorta)(-1)) and hormone replacement with 17beta-estradiol prevented this effect (159+/-29 nmol (86)Rb(+)/K(+) min(-1) (g aorta)(-1)). Na(+),K(+)-ATPase basal activity, measured as ouabain-sensitive (86)Rb(+)/K(+) uptake, was similar in male and female rats, but the effect of PE was significantly less in intact male aortas (232+/-16 in males vs 296+/-25 nmol (86)Rb(+)/K(+) min(-1) (g aorta)(-1) in females; P<0.05). Our results suggest that PE induced activation of NKCC1 and Na(+),K(+)-ATPase in the rat aorta in a gender-dependent way.

Acetylcholine↗

[Vulvar intraepithelial neoplasm].

BACKGROUND: Vulvar intraepithelial neoplasia is a challenge for the physician as it is asymptomatic and it can evolve to malignant disease. A high suspicion index, as well as some biopsies are necessary, provided an early invasive disease can exist. OBJECTIVE: To establish the patient's characteristics with vulvar intraepithelial neoplasia, seen at the Clinica de Especialidades de la Mujer, SEDENA. PATIENTS AND METHODS: An observational and retrospective analysis was done from February 1st, 1990 to December 31st, 2004. We used the data base of the Hospital Central Militar and of the Clinica de Especialidades de la Mujer, SEDENA. We identified patients with vulvar intraepithelial neoplasia or in situ vulvar cancer diagnosis. We assessed the following variables: patient's age, intraepithelial neoplasia or history of cervical cancer, acuminated vagina or condylomas, prescribed treatment and current health state. RESULTS: We identified 38 patients with ages between 49 and 82 years old. Patients with intraepithelial neoplasia I were the youngest, except one, whom at the moment of the diagnosis had 58 years old. The histopathological diagnosis was of intraepithelial neoplasia type I (koilocytotic atypia) in 10 cases, type II in 10 more, and type III in 18 of them. CONCLUSIONS: Treatment should be individual for each patient. In most of the cases and due to the high recurrence rates we prefer the conservative treatments.

Aged↗

Ca2+ transport by the synaptosomal plasma membrane Ca2+-ATPase and the effect of thioridazine.

Thioridazine inhibits the activity of the synaptic plasma membrane Ca(2+)-ATPase from pig brain and slightly decreases the rate of Ca(2+) accumulation by synaptic plasma membrane vesicles in the absence of phosphate. However, in the presence of phosphate, thioridazine increases the rate of Ca(2+) accumulation into synaptic plasma membrane vesicles. Phosphate anions diffuse through the membrane and form calcium phosphate crystals, reducing the free Ca(2+) concentration inside the vesicles and the rate of Ca(2+) leak. The higher levels of Ca(2+) accumulation obtained in the presence of thioridazine could be explained by a reduction of the rate of slippage on the plasma membrane ATPase.

Animals↗

Estradiol-induced expression of N(+)-K(+)-ATPase catalytic isoforms in rat arteries: gender differences in activity mediated by nitric oxide donors.

We tested the hypothesis that previously demonstrated gender differences in ACh-induced vascular relaxation could involve diverse Na(+)-K(+)-ATPase functions. We determined Na(+)-K(+)-ATPase by measuring arterial ouabain-sensitive 86Rb uptake in response to ACh. We found a significant increase of Na+ pump activity only in aortic rings from female rats (control 206 +/- 11 vs. 367 +/- 29 nmol 86Rb/K.min(-1).g wt tissue(-1); P < 0.01). Ovariectomy eliminated sex differences in Na(+)-K(+)-ATPase function, and chronic in vivo hormone replacement with 17beta-estradiol restored the ACh effect on Na(+)-K(+)-ATPase. Because ACh acts by enhancing production of NO, we examined whether the NO donor sodium nitroprusside (SNP) mimics the action of ACh on Na(+)-K(+)-ATPase activity. SNP increased ouabain-sensitive 86Rb uptake in denuded female arteries (control 123 +/- 7 vs. 197 +/- 12 nmol 86Rb/K.min(-1).g wt tissue(-1); P < 0.05). Methylene blue (an inhibitor of guanylate cyclase) and KT-5823 (a cGMP-dependent kinase inhibitor) blocked the stimulatory action of SNP. Exposure of female thoracic aorta to the Na+/K+ pump inhibitor ouabain significantly decreased SNP-induced and ACh-mediated relaxation of aortic rings. At the molecular level, Western blot analysis of arterial tissue revealed significant gender differences in the relative abundance of catalytic isoforms of Na(+)-K(+)-ATPase. Female-derived aortas exhibited a greater proportion of alpha2-isoform (44%) compared with male-derived aortas. Furthermore, estradiol upregulated the expression of alpha2 mRNA in male arterial explants. Our results demonstrate that enhancement of ACh-induced relaxation observed in female rats may be in part explained by 1) NO-dependent increased Na(+)-K(+)-ATPase activity in female vascular tissue and 2) greater abundance of Na(+)-K(+)-ATPase alpha2-isoform in females.

Acetylcholine↗

Effect of spermine on the activity of synaptosomal plasma membrane Ca(2+)-ATPase reconstituted in neutral or acidic phospholipids.

The activity of purified plasma membrane Ca(2+)-ATPase (PMCA) from pig brain was inhibited by spermine (a naturally occurring and highly abundant polycation in brain). The level of inhibition was dependent on the phospholipid used for reconstitution as well as on the intact or truncated state of the enzyme. An IC(50) value of 12.5 mM spermine was obtained for both, the intact protein plus calmodulin and the trypsin-digested protein, reconstituted in phosphatidylcholine (PC). In the absence of calmodulin the intact Ca(2+)-ATPase gave an IC(50) of 27 mM. This form was more sensitive to spermine inhibition when it was reconstituted with phosphatidylserine (PS), showing an IC(50) value of 2.5 mM spermine. However, the truncated form was less responsive to spermine inhibition, having an IC(50) value of 12.5 mM. Spermine has no effect on the affinity of the PMCA for Ca(2+) or ATP, but its effect on the protein is pH-dependent. It is suggested that spermine could bind to negatively charged residues on the ATPase with different accessibility, depending on the structural rearrangement of the protein. Further, when the protein is reconstituted in PS, spermine also binds to the lipid.

Adenosine Triphosphate↗