17 beta-Estradiol inhibits carotid sinus baroreceptor activity in anesthetized male rats
Abstract
Aim: To study the effect of 17beta-estradiol (E2) on carotid baroreceptor activity (CBA).
Methods: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus.
Results: E2 3, 10, and 30 micromol/L shifted FCCB to the right and downward, with a marked decrease in peak slope (PS) and peak integral value of carotid sinus nerve discharge (PIV) in a concentration-dependent manner, indicating the inhibitory effect of E2 on CBA. Pretreatment with tamoxifen (TAM) 10 micromol/L, an inhibitor of estrogen receptor, did not block the effect of E2 on CBA. Preperfusion with L-NAME 100 micromol/L, an inhibitor of NO synthase, could completely abolish the effect of E2 on CBA. NO donor SIN-1 10 micromol/L could potentiate the inhibitory effect of E2.
Conclusion: E2 inhibits CBA via endothelial NO release.
Keywords:
Methods: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in anesthetized male rats with perfused isolated carotid sinus.
Results: E2 3, 10, and 30 micromol/L shifted FCCB to the right and downward, with a marked decrease in peak slope (PS) and peak integral value of carotid sinus nerve discharge (PIV) in a concentration-dependent manner, indicating the inhibitory effect of E2 on CBA. Pretreatment with tamoxifen (TAM) 10 micromol/L, an inhibitor of estrogen receptor, did not block the effect of E2 on CBA. Preperfusion with L-NAME 100 micromol/L, an inhibitor of NO synthase, could completely abolish the effect of E2 on CBA. NO donor SIN-1 10 micromol/L could potentiate the inhibitory effect of E2.
Conclusion: E2 inhibits CBA via endothelial NO release.