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ALTERATION IN THE RELEASE OF ENDOTHELIUM‐DERIVED RELAXING FACTORS BY α‐ADRENOCEPTOR STIMULATION IN THE AORTA OF STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS
Author(s) -
Shimamura K.,
Matsuda K.,
Yamamoto K.,
Sunano S.
Publication year - 1995
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 - 10.1111/j.1440-1681.1995.tb02856.x
Subject(s) - aorta , contraction (grammar) , agonist , endothelium , clonidine , medicine , thoracic aorta , endocrinology , stimulation , chemistry , receptor
Summary 1. Endothelium‐dependent relaxation by a‐adrenoceptor agonists was examined in the thoracic aorta from normoten‐sive Wistar‐Kyoto (WKY) rats and stroke‐prone spontaneously hypertensive rats (SHRSP). 2. In ring preparations from both strains, noradrenaline‐induced contraction was increased by L‐nitro arginine (L‐NNA), a NO synthesis inhibitor. 3. L‐NNA increased the contraction induced by phenyl‐ephrine, an α 1 ‐adrenoceptor agonist. UK‐14304 and clonidine, α 2 ‐adrenoceptor agonists, did not contract the preparations with intact endothelium. However, these agents contracted preparations when NO synthesis was inhibited. 4. In a precontracted preparation, clonidine and UK‐14304 induced relaxations. The relaxations in SHRSP aorta were smaller than those in WKY aorta. 5. These results indicate that a‐agonists release NO from endothelium in WKY and SHRSP aorta. The mechanism related to NO release by α 2 ‐adrenoceptor agonist is impaired in SHRSP aorta.