The physical exercise causes a breakdown of body homeostasis, inducing metabolic, neural and humoral changes in the human body. Hormones play multiple roles at the right inner workings. The Whole Body Vibration (WBV) has become an alternative to regular physical exercise. According to the consulted literature, WBV provokes a hormonal modification that is dependent on the intrinsic characteristics of each intervention protocol. The objective of this review is to compile the most prominent scientific literature on the effects that occur in the Endocrine System (ES) of humans through the use of WBV.

O exercício físico causa um rompimento da homeostase corporal, induzindo alterações metabólicas, neurais e humorais no organismo dos seres humanos. Os hormónios desempenham diversas tarefas diretas em nosso funcionamento interno. As vibrações de corpo inteiro foram sugeridas nos últimos anos como um meio alternativo de exercício físico. De acordo com a literatura consultada, através da vibração de corpo inteiro foram encontradas alterações hormonais dependentes das características intrínsecas de cada protocolo de intervenção. O objetivo desta revisão foi reunir a literatura científica relevante sobre os efeitos que ocorrem no sistema endócrino dos seres humanos através do uso da vibração de corpo inteiro.

La realización de ejercicio físico provoca un rompimiento de la homeostasis corporal, induciendo cambios metabólicos, neurales y humorales en el organismo de los seres humanos. Las hormonas cumplen múltiples tareas en el adecuado funcionamiento interno. Las vibraciones de cuerpo completo (VCC) se han sugerido en los últimos años como un medio alternativo para la realización de ejercicio físico. Según la bibliografía consultada a través de las VCC se encuentran modificaciones hormonales dependientes de las características intrínsecas de cada protocolo de intervención. El objetivo de esta revisión es recopilar la literatura científica más destacada sobre los efectos que se producen en el sistema endocrino (SE) de humanos a través del uso de las VCC.

The use of substances for soft tissues augmentation for cosmetic purposes may produce different clinical adverse effects, including late inflammatory reactions. We report a case of a this reaction in a patient aged 41 years old female, who was infiltrated 4 years ago in both paranasal furrows and glabelar area with a polyacrylamide gel and posteriorly with botulinum toxoid type A. We discuss the main aspects of clinical and pathological processes associated with facial cosmetic procedures.

El uso de sustancias para el aumento de los tejidos blandos con fines cosméticos puede ocasionar la aparición de diferentes efectos adversos, entre los que se encuentran las reacciones inflamatorias tardías. Se presenta un caso clínico de una de estas reacciones en una paciente de 41 años de edad que había sido infiltrada 4 años antes en ambos surcos nasogenianos y glabelar con un gel de poliacrilamida y posteriormente con toxoide botulínico tipo A. Se discuten los principales aspectos clínico-patológicos de los procesos asociados a procedimientos cosméticos faciales.

This study was undertaken in anesthetized dogs to evaluate the relative participation of prostaglandins (PGs) and nitric oxide (NO) in the maintenance of total renal blood flow (TRBF), and renal medullary blood flow (RMBF). It was hypothesized that the inhibition of NO should impair cortical and medullary circulation because of the synthesis of this compound in the endothelial cells of these two territories. In contrast, under normal conditions of perfusion pressure PG synthesis is confined to the renal medulla. Hence PG inhibition should predominantly impair the medullary circulation. The initial administration of 25 µM kg-1 min-1 NG-nitro-L-arginine methyl ester produced a significant 26% decrease in TRBF and a concomitant 34% fall in RMBF, while the subsequent inhibition of PGs with 5 mg/kg meclofenamate further reduced TRBF by 33% and RMBF by 89%. In contrast, the initial administration of meclofenamate failed to change TRBF, while decreasing RMBF by 49%. The subsequent blockade of NO decreased TRBF by 35% without further altering RMBF. These results indicate that initial PG synthesis inhibition predominantly alters the medullary circulation, whereas NO inhibition decreases both cortical and medullary flow. This latter change induced by NO renders cortical and RMBF susceptible to a further decrease by PG inhibition. However, the decrease in medullary circulation produced by NO inhibition is not further enhanced by subsequent PG inhibition.

It is well known that essential hypertension evolves in most patients with "near normal" levels of plasma renin activity. However, these levels appear to be responsible for the high levels of arterial pressure because they are normalized by the administration of angiotensin II converting inhibitors or angiotensin receptor antagonist. In experimental animals, hypertension can be induced by the continuous intravenous infusion of small doses of angiotensin II that are not sufficient to evoke an immediate pressor response. However, this condition resembles the characteristics of essential hypertension because the high levels of blood pressure exist with normal plasma levels of angiotensin II. It is suggested that small amounts of angiotensin whose plasma levels are inappropriate for the existing size of extracellular volume stimulate oxidative stress which binds nitric oxide forming peroxynitrite. The latter compound oxidizes arachidonic acid producing isoprostaglandin F2a (an isoprostane) which is characterized by a strong antinatriuretic vasoconstrictor renal effect. In this chain of reactions the vasoconstrictor effects derived from oxygen quenching of nitric oxide and increased isoprostane synthesis could explain how hypertension is maintained with normal plasma levels of renin.