Abstract

Prenatal factors may program elevated blood pressure in offspring of women with polycystic ovary syndrome (PCOS). We recently determined in an experimental model of PCOS that their male offspring have elevated blood pressure compared to offspring of controls. Existing evidence shows that PCOS women may have increased renal sympathetic nerve activity (RSNA) which contributes to their elevated blood pressure. However, whether the elevated blood pressure in PCOS offspring is due to activation of the renal sympathetic nervous system (RSNS) remains undetermined. We hypothesized that activation of the RSNS contributes to the increase in blood pressure in male PCOS offspring. PCOS dams were treated with DHT pellets (DHT pellet 7.5mg/90d) beginning at 4 wks of age and continuing through pregnancy and lactation. Controls were given placebo pellets. Male PCOS offspring (mPCOS‐off) and male control offspring (mCon‐off), 20 weeks of age, were subjected to renal denervation (RD) (cutting renal nerves bilaterally and painting with 10% phenol in ethanol) or sham surgery (movement of the kidneys) (n=9/grp): mPCOS‐off‐sham, mPCOS‐off‐RD, mCon‐off‐sham, and mCon‐off‐RD, respectively. Baseline mean arterial pressure (MAP, telemetry) was significantly higher in mPCOS‐off‐sham than mCon‐off‐sham (124±1 mmHg vs. 119±1 mmHg; p<0.05). After recovery from renal denervation or sham and telemetry implantation for 14 days, MAP was decreased with renal denervation in mPCOS‐off‐RD (mPCOS‐sham: 124±1 vs mPCOS‐RD: 111±2 mmHg, p<0.05) but not in control offspring (mCon‐off‐sham: 119±1 vs mCon‐RD: 118±3 mmHg; p=NS). Thus, male PCOS offspring have an increase in MAP compared to the male control offspring, and renal denervation reduced their blood pressure, suggesting that exposure to hyperandrogenemia in utero may activate the RSNS later in life, which could contribute to high blood pressure. These data suggest that children of women with PCOS should closely monitor their blood pressure as they age to maturity.Support or Funding InformationSupported by AHA14POST18640015 and P20GM121334 (ROM).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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