Aldosterone and vascular damage

Abstract

Although the aldosterone escape mechanism is well known, aldosterone has often been neglected in the pathophysiologic consequences of the activated renin-angiotensin-aldosterone system in arterial hypertension and chronic heart failure. There is now evidence for vascular synthesis of aldosterone aside from its secretion by the adrenal cortex. Moreover, aldosterone is involved in vascular smooth muscle cell hypertrophy and hyperplasia, as well as in vascular matrix impairment and endothelial dysfunction. The mechanisms of action of aldosterone may be either delayed (genomic) or rapid (nongenomic). Deleterious effects of aldosterone leading to vascular target-organ damage include (besides salt and water retention) decreased arterial and venous compliance, increased peripheral vascular resistance, and impaired autonomic vascular control due to baroreflex dysfunction.

Mechanism for Aldosterone Potentiation of Angiotensin II–Stimulated Rat Arterial Smooth Muscle Cell Proliferation

“…However, increasing evidence suggests that modulation of blood pressure and cardiovascular homeostasis is effected not only via the effects of circulating components formed within the adrenal but also through local synthesis. 2,17,26 In the present study, clear evidence for the transcription of genes coding for both CYP11B1 and CYP11B2 was found for the first time in cultured RASMC, consistent with our previous finding of aldosterone secretion (Figure 1). Although it remains unclear how much of the steroidogenic pathway normally associated with the adrenal cortex is present, both the evidence of immunoassayable aldosterone previously obtained 18 and the actions of the 3␤-hydroxysteroid dehydrogenase inhibitor, trilostane, in the present study, indirectly support the view that steroid synthesis de novo can take place.…”

Prevalence of Primary Aldosteronism among Unselected Hypertensive Patients: A Prospective Study Based on the Use of an Aldosterone/Renin Ratio above 25 as a Screening Test

“…The fact that hybrid gene testing was positive in only one case was not surprising, given the relative rarity of that subtype, which accounts for about 0.5-1% of PA (18,21,23,32). Definitive diagnosis of GRA can only be reached by Increasing evidence has accumulated showing that excessive levels of plasma ALD are able to promote cardiac and vascular hypertrophy, remodelling and fibrosis through non-BP-dependent means (43)(44)(45)(46). The longer ALD excess is left untreated, the more severe and irreversible these cardiovascular changes become, with hypertension becoming more difficult to control and cardiovascular events more probable.…”

Participation of Prostacyclin in Endothelial Dysfunction Induced by Aldosterone in Normotensive and Hypertensive Rats

“…[1][2][3][4] To date, several studies suggested that aldosterone plays a larger role than once appreciated in the regulation of vascular tone as well as in cardiovascular alterations such as endothelial dysfunction, vascular fibrosis, and inflammation, left ventricular hypertrophy, congestive heart failure, and cardiac arrhythmias. [5][6][7][8][9][10][11][12] Furthermore, aldosterone has also been shown to be involved in the pathogenesis of hypertension. [13][14][15] In general terms, endothelial dysfunction is characterized by reduced endothelium-dependent relaxations, suggesting a reduced availability of NO attributable to a reduction of NO production or enhanced NO inactivation.…”