This study aimed to compare endothelial microcirculatory function in hypertensive and diabetic (HD) and healthy postmenopausal women before and after nasal application of 17β-estradiol.
Seventy-one women aged 42 to 59 years within 10 years of menopause, divided into HD (n = 31) and similar-age healthy (n = 40) women were evaluated noninvasively through nailfold videocapillaroscopy before and 1 hour after estradiol, measuring basal (RBCV) and maximum (RBCVmax) red blood cell velocity after 1 minute of arterial occlusion, representing baseline and endothelial-mediated vasodilation, and time to reach RBCVmax (TRBCVmax), representing microvascular compliance/stiffness.
Hot flashes did not differ from or affect microvascular results. Before estradiol, HD showed lower RBCV (1.495 ± 0.20 vs 1.52 ± 0.10 mm/s, P = 0.019), borderline lower RBCVmax (1.655 ± 0.09 vs 1.706 ± 0.10 mm/s, P = 0.054), and shorter TRBCVmax (7.94 ± 1.44 vs 8.8 ± 2.03 s, P = 0.011) compared with healthy women. After estradiol, RBCV and RBCVmax increased, and TRBCVmax decreased in both groups (P = 0.0001 for all). HD women showed a higher RBCV increment (14.6% ± 2% vs 11.1 ± 1.4%, P = 0.021) associated with a smaller TRBCVmax reduction (23.6% ± 2% vs 31% ± 2%, P = 0.045). Changes in RBCVmax did not differ between HD (11.6% ± 1%) and healthy (8.3% ± 1.3%, P = 0.1) women. RBCV, RBCVmax, and TRBCVmax absolute values after estradiol were similar between groups. Past oral contraceptive exposure (P = 0.035) and cigarette smoking (P = 0.047) influenced healthy women’s microvascular responses to estradiol, whereas triglyceride levels impaired HD vasodilation (P = 0.028).
Before estradiol, HD presented impaired microvascular dilation and compliance compared with control women of similar age. After estradiol, HD recovered microvascular endothelial-mediated dilation, reaching similar absolute values, but the smaller reduction in TRBCVmax suggests irreversible microvascular stiffness.
From the 1Laboratory for Clinical and Experimental Research on Vascular Biology–BioVasc, Biomedical Center, State University of Rio de Janeiro, Rio de Janeiro, Brazil; and 2Hospital da Lagoa, Endocrinology Sector, Health Ministry, Rio de Janeiro, Brazil.
Received July 26, 2011; revised and accepted September 29, 2011.
Funding/support: This work was supported by grants from the National Research Council of Brazil (CNPq) and the State of Rio de Janeiro Research Supporting Agency (FAPERJ).
Financial disclosure/conflicts of interest: None reported.
Address correspondence to: Ruth Clapauch, MD, PhD, Avenida das Américas 500 bloco 16 sala 228, Barra da Tijuca, Rio de Janeiro, Brazil 22631-000. E-mail: email@example.com