ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: PO1820

Salt-Induced Blood Pressure Elevation in Females Is Associated with Increased Arachidonic Acid Metabolites

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Ishimwe, Jeanne A., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Kirabo, Annet, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Elijovich, Fernando, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Ferguson, Jane F., Vanderbilt University Medical Center, Nashville, Tennessee, United States
Background

Excess dietary sodium (Na+) intake is a major risk for salt-sensitive hypertension and cardiovascular disease. Several clinical trials have found that women are more salt-sensitive than men, but the contributing sex-specific mechanisms are poorly understood. Arachidonic acid (AA) and its metabolites play a role in the pathophysiology of hypertension. We hypothesized that women have greater blood pressure (BP) elevation in response to Na+ intake that is associated with higher AA metabolites than men.

Methods

Plasma AA metabolites were measured via a metabolomics analysis in volunteers who completed a validated 3-day food record to estimate dietary Na+ intake before the study visit where BP was measured. Based on the recommendations by the American Heart Association, we classified daily Na+ intake <2.3g as normal salt, and high salt for subjects consuming ≥ 2.3g Na+. Spearman correlation was used to assess the relationship between Na+ intake and systolic blood pressure (SBP).

Results

Women (n=81) displayed a stronger relationship between BP and Na+ intake than men (n=49) (r=0.372; p<0.001 vs. r=0.317; p=0.026). The relationship between Na+ intake and BP was stronger in white (n=46, r=0.4172; p=0.004) than in black (n=22,r=0.338; p=0.124) women and conversely stronger in black (n=7, r=0.790; p=0.034) than white ( n=32, r=0.251; p=0.166) men. We measured plasma levels of palmitate and linoleate, both upstream of AA synthesis, AA, and 12-Hydroxyeicosatetraenoic acid (12-HETE) an AA metabolite. In subjects consuming a high Na+ diet (women 28, men 25) levels of linoleate (1.211 + 0.330 vs. 0.869 + 0.170; p<0.001), palmitate (1.155+ 0.292 vs. 0.924+ 0.233; p= 0.003), AA (1.119 + 0.242 vs. 0.965 + 0.201; p=0.015) and 12-HETE (1.329+ 0.925 vs. 0.902 + 0.520; p=0.0469) were higher in women. In contrast, no sex differences in any of these parameters were observed between men and women consuming a normal salt diet.

Conclusion

Our findings suggest that AA and its metabolites may account for sex and perhaps also racial differences in salt sensitivity of BP. Further study of AA and its metabolites may shed light on the mechanisms of the sex differences in salt sensitivity.

Funding

  • Other NIH Support