View clinical trials related to Hyperaldosteronism.
Filter by:This study looks at how hypertensive patients, with high levels of aldosterone (hyperaldosteronism) differ from hypertensive patients without hyperaldosteronism with regards to markers of salt appetite. It also looks at how salt appetite changes after treatment of hyperaldosteronism. Salt makes food taste good and when our bodies need salt our brains make us like salty food even more. A high salt diet contributes to hypertension and a low salt diet is an important aspect of the treatment of hypertension. Unfortunately patients find it difficult to adhere to a low salt diet. Aldosterone is produced by the adrenal glands, its release is stimulated by a salt need and it has been shown, in rodent models, to activate pathways in the brain which drive a salt appetite. Mice with enhanced activity of the aldosterone pathway in the brain become hypertensive due to increased salt intake. Hyperaldosteronism, in humans, results in hypertension. The contribution of salt appetite, as opposed to the effect of aldosterone on the kidney's retention of salt and other systems, is unknown. Human studies have shown that when a human has a salt appetite, the concentration at which they can detect the taste of salt reduces, they increase their preference for salty food, and they consume more salt. When hyperaldosteronism is suspected in a hypertensive patient, they attend hospital for a day of investigations. Patient who are shown to have hyperaldosteronism have subsequent visits for imaging of their adrenals and sampling of blood from the adrenal vein to diagnose aldosterone producing adenomas (small tumours) which may be removed surgically, if not suitable for surgery, the hyperaldosteronism is treated with medication. This study will recruit hyperaldosteronism patients to investigate the effect of aldosterone on salt appetite by testing salt taste threshold, salt taste preference and intake before and after treatment.
To investigate whether increasing water intake has renal protective effect on PA patients after surgical treatment.
Patients with primary aldosteronism, which is the most prevalent form of secondary hypertension, have an increased rate of cardiovascular events, compared to patients with essential hypertension, even with equal severity of hypertension. This might be partially attributed to the association of increased aldosterone levels with insulin resistance. How this relation can be explained from a pathophysiological point of view, is insufficiently established. Recently, microvascular dysfunction has been proposed as a link between insulin resistance and hypertension. Loss of NO-mediated vasodilation is an important feature of microvascular dysfunction; in addition, an impaired insulin-mediated microvascular NO production has been suggested to underlie the reduction in insulin-stimulated glucose disposal that is characteristic of insulin-resistant states. Increased aldosterone levels are not only associated with insulin resistance, but also with endothelial dysfunction. In addition, they interfere with the vascular effects of insulin. Therefore, the investigators hypothesize that in patients with primary aldosteronism, increased aldosterone levels induce microvascular dysfunction through reduction of NO-availability, which contributes to the development of insulin resistance, and of hypertension, in addition to the sodium-retaining effects of aldosterone.