Pedro Guevara López

Increased renal vasoconstriction and gene expression of cyclooxygenase-1 in renovascular hypertension

Vascular responses to arachidonic acid (AA) in the renal circulation are increased in hypertensive rats. We have suggested that these differences are related to changes in AA metabolism. In this study we investigated the mechanism involved in the increased AA-induced renal vasoconstriction. We evaluated vascular renal reactivity in the isolated perfused kidney, cyclooxygenase activity, protein content, and mRNA expression of kidneys from sham operated and aortic coarctation rats. Bolus injection of AA (1, 2, 4, and 8 microg) increased perfusion pressure in a dose-dependent manner by 20 +/- 4, 28 +/- 5, 38 +/- 6, and 44 +/- 7 mm Hg in sham-operated rats and 30 +/- 3, 55 +/- 5, 78 +/- 5, and 113 +/- 8 mm Hg in rats with aortic coarctation. Indomethacin (1 microg/ml) or the endoperoxide/thromboxane blocker SQ29548 (1 microM) prevented AA renal vasoconstriction. Cyclooxygenase activity, cyclooxygenase-1 protein content, and mRNA expression were also increased in the renal tissue from the aortic coarctation rats compared with sham-operated rats. In conclusion, we suggest that during development of hypertension, the cyclooxygenase-1 mRNA is induced, and consequently cyclooxygenase-1 activity and AA metabolism are increased, resulting in augmented production of vasoconstrictor prostaglandins that mediate the potentiated responsiveness to AA or other vascular agonists that release AA, thus increasing peripheral vascular resistance.

Lack of heterologous receptor desensitization induced by angiotensin II type 1 receptor activation in isolated normal rat thoracic aorta

We tested whether heterologous receptor desensitization induced by activation of AT1 receptors may explain the purported relaxation produced by angiotensin II in normal rat aorta. Also, the role for AT2 receptors in the promotion of vasodilation was studied. In endothelium-intact and endothelium-denuded aortic rings, angiotensin II elicited biphasic contractions, which were significantly depressed when repeated in each tissue. Angiotensin II produced biphasic responses on phenylephrine preconstricted endothelium-intact and endothelium-denuded tissues, without reducing precontractile tone. These responses were abolished in the presence of the AT1 receptor antagonist losartan, but no relaxing responses to angiotensin II were uncovered. PD123319 did not influence angiotensin II responses in endothelium-intact tissues precontracted with phenylephrine; thus, under AT2 receptors blockade the contractile effects of angiotensin II were not overexposed. In conclusion, angiotensin II-induced biphasic responses can be attributed to AT1 receptors activation and rapid desensitization with time. Desensitization proved to be homologous in nature, since precontractile tone induced by phenylephrine was not depressed by angiotensin II (i.e., angiotensin II did not induce heterologous α1-adrenergic receptors desensitization). We found no functional evidence of the participation of AT2 receptors in angiotensin II elicited biphasic contractions. Angiotensin II does not exert relaxant effects in normal rat aorta.

Activation of upregulated angiotensin II type 2 receptors decreases carotid pulse pressure in rats with suprarenal abdominal aortic coarctation

Abstract Our aim was to determine whether angiotensin type 2 receptors (AT2R) are involved in the depression of carotid pulse pressure (PP) in rats with suprarenal aortic coarctation (SrC). We tested the effects of losartan, PD123319, and CGP42112 on PP in SrC and Sham-operated anesthetized rats. PP increased in SrC rats. Neither losartan nor PD123319 affected PP in SrC and Sham-operated rats. CGP42112 reduced PP, in SrC rats, combined with losartan. Moreover, PD123319 blocked this effect. AT2R protein increased in the thoracic aortas of SrC rats. Thus, upregulated AT2R stimulation by CGP42112 mediates depression of PP in rats under pressure overloading.

Inhibition of PKC-dependent extracellular Ca2+ entry contributes to the depression of contractile activity in long-term pressure-overloaded endothelium-denuded rat aortas

We examined the contractile responsiveness of rat thoracic aortas under pressure overload after long-term suprarenal abdominal aortic coarctation (lt-Srac). Endothelium-dependent angiotensin II (ANG II) type 2 receptor (AT2R)-mediated depression of contractions to ANG II has been reported in short-term (1 week) pressure-overloaded rat aortas. Contractility was evaluated in the aortic rings of rats subjected to lt-Srac or sham surgery (Sham) for 8 weeks. ANG I and II levels and AT2R protein expression in the aortas of lt-Srac and Sham rats were also evaluated. lt-Srac attenuated the contractions of ANG II and phenylephrine in the aortas in an endothelium-independent manner. However, lt-Srac did not influence the transient contractions induced in endothelium-denuded aortic rings by ANG II, phenylephrine, or caffeine in Ca2+-free medium or the subsequent tonic constrictions induced by the addition of Ca2+ in the absence of agonists. Thus, the contractions induced by Ca2+ release from intracellular stores and Ca2+ influx through stored-operated channels were not inhibited in the aortas of lt-Srac rats. Potassium-elicited contractions in endothelium-denuded aortic rings of lt-Srac rats remained unaltered compared with control tissues. Consequently, the contractile depression observed in aortic tissues of lt-Srac rats cannot be explained by direct inhibition of voltage-operated Ca2+ channels. Interestingly, 12-O-tetradecanoylphorbol-13-acetate-induced contractions in endothelium-denuded aortic rings of lt-Srac rats were depressed in the presence but not in the absence of extracellular Ca2+. Neither levels of angiotensins nor of AT2R were modified in the aortas after lt-Srac. The results suggest that, in rat thoracic aortas, lt-Srac selectively inhibited protein kinase C-mediated activation of contraction that is dependent on extracellular Ca2+ entry.

Execution time Validation of the mathematical models of a electric motor in Soft Real Time simulation

This paper presents the simulation and comparison of models of first and second order of an electrical machine, in Soft Real Time. First, it describes the real-time systems and their classification. After is considered the electromechanical circuit of a Series wound DC motor, for obtaining the first and second order equations which represent the system (In continuous time and discrete time). The models obtained are simulated in SIMULINK and their parameters (electric current and angular speed) are compared between them for obtaining the relative error. Once compared the responses of the models, the execution time of the finite difference models is obtained and compared with data acquisition device execution time.

Measuring the efficiency of schedulers for Concurrent Real-time Tasks in uniprocessor systems

The schedulers for Concurrent Real-time Tasks are algorithms that are allocate in processor resources to the different tasks and at different times, in this sense, it is necessary to measure their efficiency based on the time constraints of the tasks in real time, this measurement should be performed on local and global. This paper proposes the measurement of this efficiency through the operating times and delay times of tasks and their instances.

Numerical Approaching of SIR Epidemic Model for Propagation of Computer Worms

In this paper we analyzed the model susceptible-infected-recovered (SIR); this model is based on differential equations, in this sense it cannot be implemented directly on a computer, in this context as motivation of the study presented, we propose an approximate model based on finite difference equations to achieve a simulation of the epidemic, using for this set theory and cardinality obtaining an iterative numerical method which consists on basics arithmetic operations, in addition, to be an approximate model, it will present an error due to truncation or rounding. At the end of this paper it is presented a case of study developed in SIMULINK of MATLAB software, and the results of the model based on difference equations.

Aproximación numérica del modelo epidemiológico SI para la propagación de gusanos informáticos, simulación y análisis de su error

ABSTRACT In the biological environment, there has been created epidemiological models that attempt to explain the spread dynamics of an epidemic in a population to predict the behavior of possible epidemics that can affect humanity. Based on that, this paper focused on the study of epidem-ics worms because they can spread by themselves from one infected host to the entire network of susceptible hosts. In this paper we analyzed the susceptible-infected ( SI ) model which assumes that in a community with n individuals, the num-ber of individuals in the susceptible state S ( t ) are in direct contact with the number of individuals that are in infected state I ( t ). These last individuals can spread the infection or switch to an infectious state with the factor β as a speed of infection. This model is based on differential equations so it can-not be implemented directly on a computer. Due to the complexity of this model, it is proposed an approximate model based on finite different equa-tions to achieve a simulation of the epidemic us-ing a set theory and cardinality obtaining an itera -tive numerical method which consists on basics arithmetic operations. Additionally, having in mind this is an approximate model, it will be pre-sented an error due to truncation or rounding. At the end of this paper it will be presented a case of study developed in Simulink of Matlab software, and the results of the model based on difference equations is compared with the finite-difference approximate model including the analysis of ap-proximation errors.

A metric for the evaluation of the efficiency in Scheduler of Concurrent Real-Time Tasks

The Concurrent Real-Time Tasks (TTRC), carry out all the activities of a System in Real-Time (STR); the Scheduler of Concurrent Real-Time Tasks (PTTRC) is the responsible of selecting the Real Time Task and the moment that it will take the resources, (PTTRC) is an algorithm that assigns the resources from the processor to different tasks in different moments. However, is necessary to verify effectiveness of the algorithm using an adequate approach that provides a metric between 0 and 1; the measuring should be carried out in local form and in a global way. In this work we intend the measuring of the efficiency of the scheduler through of the evolution of the instances of the Concurrent Tasks and their temporary restrictions.