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Sex Differences in Sympathetic Vasoconstrictor Responsiveness and Sympatholysis
Author(s) -
Just Timothy P,
DeLorey Darren S
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.712.4
Subject(s) - vasoconstriction , medicine , endocrinology , sympathetic nervous system , stimulation , vasodilation , femoral artery , vascular resistance , skeletal muscle , blood pressure
Sympathetic nervous system control of blood pressure and skeletal muscle vascular resistance appears to differ between males and females. The mechanism(s) responsible for sex differences in neurovascular control have not been fully elucidated. Nitric Oxide (NO) has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle and estrogen appears to modulate NO synthase (NOS) expression and NO bioavailability. The relative abundance of estrogen in females compared to males suggests that NO‐mediated inhibition of sympathetic vasoconstriction may be augmented in females relative to males. Therefore, the purpose of the present study was to investigate the hypothesis that compared to males, females would have blunted sympathetic vasoconstrictor responsiveness and augmented NO‐mediated inhibition of sympathetic vasoconstriction at rest and during exercise. Male (n=8) and Female (n=10) Sprague‐Dawley rats were anesthetized and surgically instrumented for measurement of arterial blood pressure and femoral artery vascular conductance (FVC) and stimulation of the lumbar sympathetic chain. The percentage change of FVC (%FVC) in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction before (control) and after NOS‐blockade (L‐NAME; 10 mg·kg −1 IV). At rest, vasoconstrictor responsiveness to sympathetic stimulation delivered at 2Hz was augmented (p<0.05) in females (−33 ± 8%) compared to males (−26 ± 6%), whereas vasoconstrictor responsiveness to sympathetic stimulation delivered at 5Hz was not different (p>0.05) between females (−55 ± 7%) and males (−47 ± 7%). Muscle contraction blunted (p<0.05) sympathetic vasoconstrictor responsiveness in both female and male rats; however the magnitude of sympatholysis was greater (p<0.05) in female (2Hz: 22 ± 8%; 5Hz: 30 ± 7%) compared to male (2Hz: 12 ± 6%; 5Hz: 13 ± 8%) rats. NOS blockade did not alter (p>0.05) sympatholysis of responses evoked at 2Hz in females or males; however L‐NAME reduced (p<0.05) sympatholysis of responses evoked at 5Hz in female rats. These data demonstrate that resting sympathetic vasoconstrictor responsiveness was augmented in female rats compared to male rats in a stimulation frequency‐dependent manner. Furthermore, sympatholysis was enhanced in female compared to male rats and this was partly attributable to augmented NO‐mediated inhibition of sympathetic vasoconstriction. Support or Funding Information Natural Sciences and Engineering Research Council of Canada (NSERC), Canadian Foundation for Innovation, and Alberta Advanced Education and Technology.