Is Hypertension a Disorder of Volume Control? What Is the Evidence?

Abstract

The etiological factors responsible for the hypertensive phenotype are complex and several experimental and clinical observations point to a major role of the kidney as being responsible. Genetic studies of uncommon diseases which express monogenetic inheritance all have in common a dysregulation of Na⁺ balance and volume expansion. Furthermore, epidemiological data suggest an increased incidence of hypertension in communities with high excretory rates of Na⁺. Experimental data also suggest that low birth weight is associated with an increase in the frequency of hypertension later in life and raises the possibility that intrauterine imprinting may contribute to the expression of the phenotype. Upregulation of the Na⁺/K⁺/2Cl^– and thiazide-sensitive transporters in low birth weight animals may provide the physiological basis for these observations. In addition, low birth weight is associated with a decrease in nephron number. Therefore, low nephron number may induce adaptive changes in utero which influence volume homeostasis later in life and subtle gain of function mutations in one or more of these transporters may unmask defects in volume homeostasis with increasing salt intake. Finally, the high prevalence of hypertension in functionally anephric patience seems to respond to sustained maintenance of ‘dry weight’ through ultrafiltration.

The Role of Stress and Its Hormonal Mediators in the Ontopathogeny of Cardiovascular Disorders

“…However, at present the main mortality is caused by cardiovascular (CV) diseases, what augments the necessity of describing the role of stress and its mediators in the etiopathogeny of such diseases. Moreover, among the CV disorders, systemic arterial hypertension is saliently important as highly prevalent disorder and one of the principal risk factors for ischemic heart disease and stroke, as well as heart or kidney insufficiency [3], thus explaining our intention to devote more space in this article for hypertension.…”

Efeito da espironolactona sobre a função e morfologia renal de ratos hipertensos por infusão crônica de Angiotensina II.

“…O SRA (Figura 1) é representado como uma cascata biológica multienzimática, na qual o angiotensinogênio é o substrato mais importante. A síntese de Ang II é iniciada e principalmente regulada pela renina, enzima sintetizada essencialmente pelas células justaglomerulares renais, (MINDEL;MORRISON, 2005;YOO et al, 2007). A renina cliva o angiotensinogênio circulante, produzido principalmente no fígado, para liberar o decapeptídeo angiotensina I, que por sua vez, sofre ação da enzima conversora de angiotensina I (ECA) e libera o octapeptídeo ativo, angiotensina II.…”