Polycystic ovary syndrome potentiates blood pressure and vascular responses to the cold pressor test.

Polycystic ovary syndrome (PCOS) predisposes women to cardiovascular diseases. Blood pressure (BP) responses to the cold pressor test (CPT) predict future cardiovascular risk but have yet to be characterized in PCOS. Therefore, we compared BP responses to the CPT between females with PCOS [n = 10; age: 22 ± 3 yr, body mass index (BMI): 23.9 ± 3 kg/m²] and healthy controls (CTRL; n = 10; age: 22 ± 2 yr, BMI: 22.1 ± 2 kg/m²). BP (finger photoplethysmography calibrated to manual sphygmomanometry-derived values), femoral blood flow (duplex ultrasound), and vascular resistance [FVR; mean arterial pressure (MAP)/blood flow] were measured continuously at baseline and across a 3-min hand CPT. Venous blood samples were used to quantify the free androgen index (FAI; total testosterone/sex hormone binding globulin × 100). Baseline MAP was not different between PCOS and CTRL (87 ± 7 vs. 82 ± 11 mmHg, respectively; P = 0.25), nor was systolic BP (SBP; 109 ± 9 vs. 106 ± 7 mmHg; P = 0.42). Across the CPT, MAP and SBP were higher in PCOS than CTRL (main effects of group, both P < 0.05). Peak CPT induced increases in MAP (+12 ± 5 vs. +7 ± 4 mmHg; P = 0.04) and corresponding changes in SBP (+13 ± 7 vs. +7 ± 3 mmHg; P = 0.04) and FVR (+0.17 ± 0.08 vs. +0.02 ± 0.13 mmHg/mL/min; P = 0.01) were larger in PCOS than CTRL. Within-group regressions indicated that FAI was positively associated with relative increases in peak MAP (R² = 0.72, P < 0.01) and corresponding changes in FVR (R² = 0.83, P < 0.01) in females with PCOS but not in CTRL (MAP: R² = 0.03, P = 0.62; FVR: R² = 0.12, P = 0.41). Young, lean females with PCOS demonstrate exaggerated BP and vascular responses to the CPT that may be indicative of elevated cardiovascular risk mediated in part by the detrimental effects of elevated androgens.NEW & NOTEWORTHY Young, lean, and otherwise healthy females with polycystic ovary syndrome (PCOS) demonstrated exaggerated blood pressure responses to the cold pressor test (CPT) relative to controls. CPT responses were associated with bioavailable androgens, suggesting that hyperandrogenism contributes to exaggerated responses to the CPT in PCOS. Given associations between CPT responsiveness and the subsequent development of hypertension, these findings add to mounting evidence for increased cardiovascular risk even in lean females with PCOS.