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ACUTE EXPOSURE TO A LOW LEVEL OF TESTOSTERONE IMPAIRS RELAXATION IN PORCINE CORONARY ARTERIES
Author(s) -
Quan ADRIAN,
Teoh HWEE,
Man RICKY YK
Publication year - 1999
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.1999.03138.x
Subject(s) - testosterone (patch) , medicine , sodium nitroprusside , endocrinology , bradykinin , coronary artery disease , chemistry , nitric oxide , receptor
SUMMARY 1. While the gender bias associated with coronary artery disease has been suggested to be partially accounted for by the protective effects of oestrogens, the role of testosterone remains unclear. The aim of the present study was to determine whether vasorelaxation could be affected by acute administration of testosterone with and without 17β‐oestradiol. 2. Precontracted porcine coronary artery rings were relaxed with sodium nitroprusside (SNP), levcromakalim, bradykinin (BK) or A23187. At 1 nmol/L, testosterone impaired relaxations to BK and A23187, while the same concentration of 17β‐oestradiol potentiated levcromakalim‐ and SNP‐induced relaxations. The impairment of relaxation responses by testosterone was reduced in the presence of 17β‐oestradiol, while the enhancement by 17β‐oestradiol was decreased by testosterone. 3. We demonstrate that a low level of testosterone can impair agonist‐induced relaxation, an effect that is reduced by 17β‐oestradiol. This further supports evidence indicating a detrimental role for testosterone in coronary artery disease and suggests that circulating levels of testosterone may undermine the beneficial effects of oestrogen in women.