Estrogen, natriuretic peptides and the renin-angiotensin system.
There are significant gender-specific differences in the incidence of hypertension and the clinical outcome of cardiovascular disease between premenopausal women and age-matched men, suggesting that sex hormones such as estrogen (E) might be responsible for the observed cardioprotective effects. This cardioprotective action of E is thought to involve lipoproteins. However, the effect of E on the lipid profile accounts for about 50% of the reduction in cardiovascular disease, indicating that there might be other mechanisms by which E exerts its cardioprotective effects. At present, the underlying mechanism of E action is poorly understood. In this review, the interplay between E, the natriuretic peptides (NP) and the renin-angiotensin system (RAS) is examined. It is hypothesized that E might, through endocrine and/or paracrine action, modulate cardiac NP in females by affecting the RAS either directly or indirectly.
Kuroski de Bold
M L
ML
Department of Pathology, University of Ottawa Heart Institute, ON, Canada. mercedes@uottawa.ca
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000378:metabolism*; D004967:Estrogens / Q000378:metabolism*; D005260:Female; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D020097:Natriuretic Peptide, Brain / Q000378:metabolism; D051381:Rats; D011960:Receptors, Estrogen / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000502:physiology*; D013739:Testosterone / Q000378:metabolism
D004967:Estrogens; D011960:Receptors, Estrogen; D020097:Natriuretic Peptide, Brain; D013739:Testosterone; D009320:Atrial Natriuretic Factor