Journal article
Central oxytocin systems may mediate a cardiovascular response to acute stress in rats
American journal of physiology. Heart and circulatory physiology, Vol.256(5), pp.H1369-H1377
1989
DOI: 10.1152/ajpheart.1989.256.5.H1369
Abstract
The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.
Details
- Title: Subtitle
- Central oxytocin systems may mediate a cardiovascular response to acute stress in rats
- Creators
- Michael F Callahan - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United StatesRobert F Kirby - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United StatesJ. Thomas Cunningham - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United StatesShawnee L Eskridge-Sloop - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United StatesAlan K Johnson - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United StatesRichard Mccarty - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United StatesKenneth A Gruber - Wake forest univ. medical cent., dep. medicine, Winston-Salem NC 27103, United States
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.256(5), pp.H1369-H1377
- Publisher
- American Physiological Society
- DOI
- 10.1152/ajpheart.1989.256.5.H1369
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 1989
- Academic Unit
- Neuroscience and Pharmacology; Health and Human Physiology; Psychological and Brain Sciences
- Record Identifier
- 9984213429102771
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