Metabolic syndrome (MS) is composed of several metabolic abnormalities that increase the risk of cardiovascular diseases and diabetes. Although there are treatments for the components of MS, this pathology maintains a high mortality,... more
Metabolic syndrome (MS) is composed of several metabolic abnormalities that increase the risk of cardiovascular diseases and diabetes. Although there are treatments for the components of MS, this pathology maintains a high mortality, suggesting that there are other mechanisms in which orphan receptors such as GPR26 and GPR39 may be involved. For this reason, the aim of this work was to evaluate the expression of GPR26 and GPR39 orphan receptors in two models of MS (diet and genetics). We used male Wistar rats, which received 70% fructose in drinking water for 9 weeks, and obese Zucker rats. We measured weight, blood pressure, glucose, triglycerides, total cholesterol, HDL cholesterol, LDL cholesterol to determine the MS and the expression of the orphan receptors GPR26 and GPR39 in brain, heart, aorta, liver, and kidney by RT-PCR. The analysis of the expression of the orphan receptors GPR26 and GPR39 showed that the receptors are expressed in some tissues, but the expression of the G...
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The aim of this study was to investigate the possible relationship among insulin resistance (IR), endothelial dysfunction, and alteration of adipokines in Mexican obese adolescents and their association with metabolic syndrome (MetS). Two... more
The aim of this study was to investigate the possible relationship among insulin resistance (IR), endothelial dysfunction, and alteration of adipokines in Mexican obese adolescents and their association with metabolic syndrome (MetS). Two hundred and twenty-seven adolescents were classified according to the body mass index (BMI) (control: N=104; obese: N=123) and homeostasis model of the assessment-insulin resistance index (HOMA-IR) (obese with IR: N=65). The circulating concentrations of leptin, adiponectin, soluble intercellular adhesion molecule-1 (sICAM-1), and IR were determined by standard methods. The obese adolescents with IR presented increased presence of MetS and higher circulating concentrations in sICAM-1 in comparison with the obese subjects without IR. The lowest concentrations of adiponectin were observed in the obese with IR. In multivariate linear regression models, sICAM-1 along with triglycerides, total cholesterol, and waist circumference was strongly associated with HOMA-IR (R(2)=0.457, P=0.008). Similarly, after adjustment for age, BMI-SDS, lipids, and adipokines, HOMA-IR remained associated with sICAM-1 (R(2)=0.372, P=0.008). BMI-SDS was mildly associated with leptin (R(2)=0.176, P=0.002) and the waist circumference was mild and independent determinant of adiponectin (R(2)=0.136, P=0.007). Our findings demonstrated that the obese adolescents, particularly the obese subjects with IR exhibited increased presence of MetS, abnormality of adipokines, and endothelial dysfunction. The significant interaction between IR and endothelial dysfunction may suggest a novel therapeutic approach to prevent or delay systemic IR and the genesis of cardiovascular diseases in obese patients.
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Hypertension and diabetes are multifactorial diseases that frequently coexist and exacerbate each another. During the development of diabetes, the impairment of noradrenergic and renin-angiotensin systems has been reported in the response... more
Hypertension and diabetes are multifactorial diseases that frequently coexist and exacerbate each another. During the development of diabetes, the impairment of noradrenergic and renin-angiotensin systems has been reported in the response mediated by α1-AR and AT1 receptors. Although their participation in the development of cardiovascular complications is still controversial, some studies have found increased or diminished response to the vasoconstrictive effect of noradrenaline or angiotensin II in a time-dependent manner of diabetes. Thus, the aim of this work was to investigate the possible changes in the expression or localization of α1-AR (α1A and α1D) and angiotensin II receptors (AT1 and AT2) in aorta of rats after 4 weeks of the onset of diabetes. In order to be able to examine the expression of these receptors, immunofluorescence procedure was performed in tunica intima and tunica media of histological sections of aorta. Fluorescence was detected by a confocal microscopy. ...
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... II. Auteur(s) / Author(s). VILLALON CM ; TERRON JA ; HONG E. ; SAXENA PR ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s). ... Aparato circulatorio. ; Localisation / Location. INIST-CNRS,Cote INIST : 3481,... more
... II. Auteur(s) / Author(s). VILLALON CM ; TERRON JA ; HONG E. ; SAXENA PR ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s). ... Aparato circulatorio. ; Localisation / Location. INIST-CNRS,Cote INIST : 3481, 35400004915055.0100. Nº notice refdoc (ud4) : 4006409. ...
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The present study was designed to analyze the effects of drugs that interfere with sympathetic transmission on the external carotid vasodilator response induced by the 5-HT1A receptor agonist, indorenate, in pentobarbital-anesthetized... more
The present study was designed to analyze the effects of drugs that interfere with sympathetic transmission on the external carotid vasodilator response induced by the 5-HT1A receptor agonist, indorenate, in pentobarbital-anesthetized dogs. Intracarotid (i.c.) infusions of indorenate (1000 micrograms/l min) produced an increase in external carotid blood flow (external C.B.F.) without modifying mean arterial blood pressure or heart rate. This effect of indorenate was dose-dependently antagonized by intravenous (i.v.) administration of the alpha 1-adrenoceptor antagonist, prazosin (1, 3.1, 10, 31 and 100 micrograms/kg), the ganglionic blocking agent, mecamylamine (0.031, 0.1, 0.31, 1, 3.1 and 10 mg/kg) or the 5-HT2 receptor and alpha 1-adrenoceptor antagonist, ketanserin (10, 31 and 100 micrograms/kg). It is concluded that indorenate-induced increase in canine external C.B.F. is dependent on the vascular neurogenic tone.
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This study was to investigate whether the metabolic abnormalities of adipokines and asymmetrical dimethylarginine (ADMA) associate with pulmonary function deficits in adolescents with obesity and asthma. This study enrolled 28 obese... more
This study was to investigate whether the metabolic abnormalities of adipokines and asymmetrical dimethylarginine (ADMA) associate with pulmonary function deficits in adolescents with obesity and asthma. This study enrolled 28 obese adolescents with asthma, 46 obese adolescents without asthma, 58 normal-weight adolescents with asthma, and 63 healthy control subjects. Serum levels of leptin, high-molecule-weight (HMW) adiponectin, retinol binding protein 4 (RBP4), asymmetrical dimethylarginine (ADMA), and pulmonary function were qualified. The obese subjects had higher levels of leptin and ADMA but lower levels of HMW adiponectin than the normal-weight subjects with or without asthma. The subjects with asthma had higher levels of RBP4 than those without asthma. The obese adolescents with asthma had lowest forced expiratory lung volume in the first second (FEV1)/forced vital capacity (FVC) ratio among the four study groups. In all the study subjects and in the subjects with asthma alone, the FEV1/FVC ratio associated negatively with leptin, however, such association was rendered non-significant when adjusted for BMI. The pulmonary function deficits associated inversely with BMI percentile in the subjects with asthma. However, the decreased FEV1/FVC ratio was not correlated with HMW adiponectin, RBP4 or ADMA. Our present study confirmed obstructive pattern of pulmonary function characterized by the reduced FEV1/FVC ratio in the obese adolescents with asthma. These pulmonary deficits were associated inversely with the increased BMI percentile.
Research Interests: Asthma, Adolescent, Humans, Child, Female, and 8 moreMale, Leptin, Lung, Clinical Sciences, Adipokines, Adiponectin, Arginine, and Pediatric Obesity
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Spinal cord injury (SCI) produces multiple systemic and metabolic alterations. Although some systemic alterations could be associated with ischemic organ damage, little is known about microvascular blood flow (MVBF) in organs other than... more
Spinal cord injury (SCI) produces multiple systemic and metabolic alterations. Although some systemic alterations could be associated with ischemic organ damage, little is known about microvascular blood flow (MVBF) in organs other than the spinal cord after acute SCI. We used laser Doppler flowmetry in anesthetized rats to assess MVBF in several tissues before and after complete T-2 and T-9 SCI at 1 h and on days 1, 3, and 7 post-SCI. Mean arterial blood pressure (MAP), heart rate and hematologic variables also were recorded. MAP changes after T-2 injury were not significant, while MAP decreased significantly 1 h after T-9 injury. Statistically significant bradycardia occurred after T-2 injury at 7 days; statistically significant tachycardia occurred after T-9 injury at 1, 3, and 7 days. Hematocrit significantly increased at day 1 and decreased at days 3 and 7 after T-2 injury. SCI was associated with significant decreases in MVBF in liver, spleen, muscle and fore footpad skin. Changes in MVBF in hind footpad skin and kidney were not significant. Changes were more pronounced at 1 h and 1 day post-SCI. Significant differences between MVBF after T-2 and T-9 SCI occurred only in liver. MVBF significantly correlated with regional peripheral vascular resistances (assessed using the MAP/MVBF ratio), but not with MAP. In conclusion, organ-specific changes in systemic MVBF that are influenced by the level of SCI, could contribute to organ dysfunction.
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ABSTRACT
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We investigated whether fenofibrate, metformin, and their combination generate cardioprotection in a rat model of type 2 diabetes (T2D) and acute myocardial infarction (AMI). Streptozotocin-induced diabetic- (DB-) rats received 14 days of... more
We investigated whether fenofibrate, metformin, and their combination generate cardioprotection in a rat model of type 2 diabetes (T2D) and acute myocardial infarction (AMI). Streptozotocin-induced diabetic- (DB-) rats received 14 days of either vehicle, fenofibrate, metformin, or their combination and immediately after underwent myocardial ischemia/reperfusion (I/R). Fenofibrate plus metformin generated cardioprotection in a DBI/R model, reported as decreased coronary vascular resistance, compared to DBI/R-Vehicle, smaller infarct size, and increased cardiac work. The subchronic treatment with fenofibrate plus metformin increased, compared with DBI/R-Vehicle, total antioxidant capacity, manganese-dependent superoxide dismutase activity (MnSOD), guanosine triphosphate cyclohydrolase I (GTPCH-I) expression, tetrahydrobiopterin : dihydrobiopterin (BH4 : BH2) ratio, endothelial nitric oxide synthase (eNOS) activity, nitric oxide (NO) bioavailability, and decreased inducible NOS (iNOS) activity. These findings suggest that PPARα activation by fenofibrate + metformin, at low doses, generates cardioprotection in a rat model of T2D and AMI and may represent a novel treatment strategy to limit I/R injury in patients with T2D.
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The effect of acute hyperglycemia on blood pressure has seldom been explored. We investigated the effect of oral glucose administration on arterial blood pressure. We used male Wistar rats that received oral glucose (3, 6 or 12g/kg p.o.).... more
The effect of acute hyperglycemia on blood pressure has seldom been explored. We investigated the effect of oral glucose administration on arterial blood pressure. We used male Wistar rats that received oral glucose (3, 6 or 12g/kg p.o.). Blood pressure was registered using telemetry. The three doses produced an increase in the mean arterial pressure and the effect was greater
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Research Interests: Neuroscience, Psychology, Cognitive Science, Spinal Cord Injury, Antioxidants, and 17 moreHemodynamics, Nitric oxide, Animals, Spinal Cord, Male, Glutathione, Heart rate, Catalase, Superoxide Dismutase, Lipid peroxidation, Rats, Rat, Oxidative Damage, Benzoic Acid, Spinal Cord Injuries, Neurosciences, and Nitric oxide donors
... Vol. 148, No. 1 Printed in USA PHARMACOLOGY OF A GROUP OF PHENYLPIPERAZINE TETRAZOLE DERIVATIVES WITH ADRENERGIC BLOCKING ACTIONS 11OJ)OLFO RODRIGUEZ, ENRIQUE HONG, HORACIO V1DRIO AND EFRATN G. PARDO ...
Research Interests: Pharmacology, Research, Cats, Smooth muscle, Epinephrine, and 4 moreBlood Pressure, Heart, Rabbits, and Aorta
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Page 1. 303 TIIR JOURNAL OF I'iiARMACOLOGY AND EXPRRIMENTAL THERAPEUrLCe Copyright © 1967 by The Williams & Wilkins Co. AUTOINHIBITION IN RABBIT AORTIC STRIPS AFTER EPINEPHRINE' EFRAIN G. PARDO, ENRIQUE HONG AND... more
Page 1. 303 TIIR JOURNAL OF I'iiARMACOLOGY AND EXPRRIMENTAL THERAPEUrLCe Copyright © 1967 by The Williams & Wilkins Co. AUTOINHIBITION IN RABBIT AORTIC STRIPS AFTER EPINEPHRINE' EFRAIN G. PARDO, ENRIQUE HONG AND JACQUES LELORIER' ...
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Base de dados : LILACS. Pesquisa : 177057 [Identificador único]. Referências encontradas : 1 [refinar]. Mostrando: 1 .. 1 no formato [Detalhado]. página 1 de 1, 1 / 1, LILACS, seleciona. para imprimir. Fotocópia. experimental, Documentos... more
Base de dados : LILACS. Pesquisa : 177057 [Identificador único]. Referências encontradas : 1 [refinar]. Mostrando: 1 .. 1 no formato [Detalhado]. página 1 de 1, 1 / 1, LILACS, seleciona. para imprimir. Fotocópia. experimental, Documentos relacionados. Id: 177057. ...
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Research Interests: Dogs, Female, Animals, Male, Norepinephrine, and 4 moreRats, Vasodilation, Serotonin antagonists, and Piperidines
Activation of rabbit aortic strips with alpha adrenergic agonists increased the labeling (with [32P]Pi) of phosphatidylinositol (PI) and phosphatidic acid and contracted the vascular preparations in dose-related fashion. Epinephrine,... more
Activation of rabbit aortic strips with alpha adrenergic agonists increased the labeling (with [32P]Pi) of phosphatidylinositol (PI) and phosphatidic acid and contracted the vascular preparations in dose-related fashion. Epinephrine, norepinephrine and methoxamine produced maximal effects, whereas clonidine behaved as partial agonist and B-HT 933 (2-amino-6-ethyl-4,5,7,8-tetrahydro-6H-oxazole-[5,4-d] azepin dihydrochloride) was almost without activity in the two experimental models used. Phenylephrine was a full agonist in producing contraction, but failed to elicit the maximal increase in PI labeling. The EC50 values to produce contraction of aortic strips were lower for all agonists than those required to increase the incorporation of radioactive phosphate into PI, but there was a good correlation between the two sets of data. The increased PI labeling and contraction of aortic strips induced by epinephrine were antagonized by prazosin and yohimbine in dose-related fashion, but the first alpha blocker was about three orders of magnitude more potent than the second in antagonizing the two effects. The present results indicate that both stimulation of PI labeling and contraction are mediated through activation of alpha-1 adrenoceptors in rabbit aorta.
Research Interests: Pharmacology, Kinetics, Phospholipids, Phosphorus, Epinephrine, and 16 moreBeta decay, Female, Animals, Male, Cardiovascular system, Dose Response Relationship, Phosphoric acid, Muscle contraction, Phosphoric Acid, Rabbits, Reaction Kinetics, Blood Vessel, Organic Compound, Phosphatidic acid, Experimental Model, and Prazosin
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The aim of this study was to provide further evidence about the participation of alpha 1-adrenoceptors in the vascular responses elicited by ipsapirone. This 5-HT1A agonist displayed vasodilator activity only when aortic rings were... more
The aim of this study was to provide further evidence about the participation of alpha 1-adrenoceptors in the vascular responses elicited by ipsapirone. This 5-HT1A agonist displayed vasodilator activity only when aortic rings were precontracted by alpha-adrenergic compounds. The relaxant effect was particularly evident when rings were precontracted with methoxamine (selective alpha 1A-adrenergic agonist). On the other hand, ipsapirone but not chloroethylclonidine (selective alpha 1B-adrenergic antagonist), clearly displaced norepinephrine and methoxamine vasocontractile concentration-response curves to the right. Finally, ipsapirone protected the alpha-adrenoceptors form the irreversible blockade provoked by phenoxybenzamine, as judged by the norepinephrine contraction and stimulated phosphatidylinositil labeling. Accordingly the relaxant effect elicited by ipsapirone in aortic rings precontracted with alpha-adrenergic agonists and the protective action against blockade by phenoxybenzamine shown by this agent are proof of its ability to occupy alpha 1-adrenoceptors. Specifically, alpha 1A-adrenergic receptors seem to be involved in ipsapirone vascular effects, since this agent selectively relaxed aortic preparation precontracted with methoxamine and unlike chloroethylclonidine, clearly inhibited the contractile effect of this agonist. In summary, the present findings can be explained by accepting that ipsapirone may act as an antagonist at alpha 1A-adrenoceptors.
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Pelanserin pharmacokinetics were studied in six normotensive dogs after intravenous and oral administration. Additionally, the relationship between pelanserin plasma levels and its antihypertensive effect was studied in six hypertensive... more
Pelanserin pharmacokinetics were studied in six normotensive dogs after intravenous and oral administration. Additionally, the relationship between pelanserin plasma levels and its antihypertensive effect was studied in six hypertensive dogs after a single oral administration. Plasma level-time curves were fitted to an open two compartments model. Pelanserin bioavailability after oral dosing was about 30%, this could be due to a poor absorption from the gastrointestinal tract or to an important hepatic biotransformation by first pass effect. On the other hand, oral administration of pelanserin resulted in a significant antihypertensive effect that was not followed by tachycardia. Pelanserin plasma levels did not significantly correlate with the obtained antihypertensive effect. These results suggest that the observed effect was not only due to an action at peripheral level, but other mechanisms could likely be involved, probably with participation of the central nervous system. The pharmacokinetic and pharmacodynamic profiles of pelanserin allow to predict that this drug could have a place in the therapeutics of arterial hypertension.