Stress‐induced Salt Sensitivity is Modulated by Angiotensin II
Authors: Jeong Jin Hee , Harris Ryan A. , Hanevold Coral , Harshfiled Gregory 
Published: June 2021

Intro

Increased sensitivity of blood pressure (BP) to dietary sodium (“salt‐sensitivity”) has been described to partially explain the etiology of hypertension (HTN) in African‐Americans (AAs). Our group has demonstrated a form of salt sensitivity that is induced by mental stress rather than by dietary sodium in a significant percentage of AAs. The underlying mechanism for stress‐induced salt‐sensitivity in AAs has yet to be described. However, animal models provide evidence that it results from increased renal sympathetic nerve activity (SNA) that triggers renal sodium reabsorption through the action of angiotensin II (Ang II).

Aim

Our study sought to test the hypothesis that mental stress‐induced impaired regulation of sodium and subsequent changes in BP are mediated by the action of Ang II in normotensive AAs.

Methods

Utilizing a double‐blind, randomized and cross‐over study design, 132 normotensive AAs (25±7 yr) were placed on a controlled sodium diet for 7 days and were treated concomitantly with either a placebo or irbesartan (an Ang II receptor blocker; ARB) in random order. A mental stress by competitive video game challenges were used to provoke the stress response on the final day of each treatment. Urinary sodium excretion (UNaV), blood pressure (BP), total peripheral resistance (TPR) and heart rate (HR) were collected before, during, and 1‐hr after the stress.

Results

BP measured every 15 minutes stayed elevated throughout the stress period on placebo, whereas the stress‐induced increase in BP was delayed on ARB day (p=0.024 for Treatment × Time interaction). ARB treatment also resulted in lower BP and TPR at rest, stress and recovery (p>0.05 for all). Notably, systolic BP at the end of recovery on ARB was significantly lower compared to the placebo (109.8 ±13.3 vs 117.4 ± 12.3 mmHg respectively; p<0.001) and was also significantly decreased from the pre‐stress level (mean difference; −1.9 ±9.4 mmHg; p=0.02). In response to stress, UNaV, BP and HR were all increased in each of placebo and ARB day. However, 30.2% of subjects retained sodium during stress despite an increase in BP on placebo. ARB treatment increased ΔUNaVstress − rest among the sodium retainers (−1.14 ±5.95 mEq/min on placebo, 7.63±9.64 mEq/min on ARB, p=0.001) without changes in UNaV at rest and recovery.

Conclusion

The use of ARBs in AAs is controversial despite an unsatisfactory efficacy of the current first line of HPT therapy in AAs. Our data demonstrates that suppression of Ang II, by using ARB, blunted the stress‐induced sodium retention, attenuated BP reactivity to stress and improved post‐stress BP recovery process in AAs. These confirm the Ang II‐dependent antinatriuretic actions in the process of stress responses on renal SNA. Thus, treatment approaches that antagonize Ang II's actions could have significant relevance to potentially lower susceptibility to stress‐induced dysregulation of sodium and BP and eventually the premature development of salt‐sensitive HTN in AAs.

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.