Clinical Trials Directory

Trials / Withdrawn

WithdrawnNCT02096939

Microvascular Function in Primary Aldosteronism

Microvascular Function in Patients With Primary Aldosteronism and Essential Hypertension

Status
Withdrawn
Phase
Study type
Observational
Enrollment
0 (actual)
Sponsor
Maastricht University Medical Center · Academic / Other
Sex
All
Age
18 Years – 70 Years
Healthy volunteers
Not accepted

Summary

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.

Conditions

Interventions

TypeNameDescription
PROCEDUREAdrenal extirpation
DRUGAntihypertensive medication

Timeline

Start date
2014-09-01
Primary completion
2016-04-01
Completion
2016-04-01
First posted
2014-03-26
Last updated
2015-08-25

Source: ClinicalTrials.gov record NCT02096939. Inclusion in this directory is not an endorsement.