This review highlights the mechanistic role of androgens in cardiovascular dysfunction and hypertension in PCOS, noting significant discrepancies between preclinical models and human studies.
Polycystic ovary syndrome (PCOS) is the most common endocrinopathy in premenopausal females. The condition is associated with an increased prevalence of cardiovascular risk factors, including hypertension. Observational studies report that some blood pressure control mechanisms are altered in PCOS compared to controls (sympathetic nervous system activity, endothelial and vasodilator function, renin angiotensin aldosterone system activation), and that these impairments correlate with androgen hormone levels, which are chronically elevated in the condition. As such, hyperandrogenism is the proposed locus of origin for the link between PCOS and cardiovascular dysfunction, yet the underlying mechanisms remain poorly understood. Preclinical work has provided some insight into how androgens modulate blood pressure control in PCOS. However there are marked discrepancies between the effects of androgens in cellular and tissue studies versus in vivo animal and human PCOS studies. This may be related to the heterogeneity of the preclinical models and samples used in this research and whether preclinical work is modelling hyperandrogenism in physiologically relevant terms for PCOS. This review collates preclinical and clinical evidence to summarise what is known and what remains unknown about cardiovascular control mechanisms in PCOS. We examine aspects of blood pressure regulation that are altered in other hypertensive cohorts, presenting current evidence for a mechanistic role of androgens on these systems, while acknowledging the diverse experimental models and participant cohorts from which the results are derived.
Adams et al. (Thu,) studied this question.