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Central vagal activation by alpha 2 ‐adrenergic stimulation is impaired in spontaneously hypertensive rats
Author(s) -
Kawada T.,
Akiyama T.,
Shimizu S.,
Kamiya A.,
Uemura K.,
Sata Y.,
Shirai M.,
Sugimachi M.
Publication year - 2012
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2012.02439.x
Subject(s) - stimulation , adrenergic , medicine , endocrinology , anesthesia , receptor
Aim To elucidate the abnormality of vagal control in spontaneously hypertensive rats ( SHR ) by measuring left ventricular myocardial interstitial acetylcholine ( AC h) release in response to α 2 ‐adrenergic stimulation as an index of in vivo vagal nerve activity. Methods A cardiac microdialysis technique was applied to the rat left ventricle in vivo , and the effect of α 2 ‐adrenergic stimulation by medetomidine or electrical vagal nerve stimulation on myocardial interstitial AC h levels was examined in normotensive Wistar–Kyoto rats ( WKY ) and SHR under anaesthetized conditions. Results Intravenous medetomidine (0.1 mg kg −1 ) significantly increased the AC h levels in WKY (from 2.4 ± 0.6 to 4.2 ± 1.3 nmol L −1 , P < 0.05, n = 7) but not in SHR (from 2.5 ± 0.7 to 2.7 ± 0.7 nmol L −1 , n = 7). In contrast, electrical vagal nerve stimulation increased the AC h levels in both WKY (from 1.0 ± 0.4 to 2.9 ± 0.9 nmol L −1 , P < 0.001, n = 6) and SHR (from 0.9 ± 0.2 to 2.2 ± 0.4 nmol L −1 , P < 0.001, n = 6). Intravenous administration of medetomidine (0.1 mg kg −1 ) did not affect the vagal nerve stimulation–induced AC h release in either WKY or SHR . Conclusion Medetomidine‐induced central vagal activation was impaired in SHR , whereas peripheral vagal control of AC h release was preserved. In addition to abnormal sympathetic control, vagal control by the central nervous system may be impaired in SHR .