Central oxytocin systems may mediate a cardiovascular response to acute stress in rats

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.

Sinoaortic Denervation Does Not Increase Cardiovascular/ Endocrine Responses to Stress

“…Three to five days before stress testing, the rats were anesthetized with ketamine:xylazine (50:10 mg/kg, i.m. ), and a carotid artery catheter was inserted as pre viously described [15]. This catheter was fashioned ofTDMAC-heparin (tridodecylmethyl-ammonium chloride-heparin, 2% solution: Polysciences, Inc., Warrington, Pa.) impregnated silastic tubing fused to drawn PE-60.…”

Intergenerational effects of cocaine on maternal aggressive behavior and brain oxytocin in rat dams

“…In addition to an association of oxytocin with MA, the stress response has also been strongly associated with oxytocin (Callahan et al 1989;Uvnas-Moberg et al 1994;Jezova et al 1995;Nishioka et al 1998;Uvnas-Moberg 1998;Neumann et al 2001;Amico et al 2004), a relationship that has been increasingly studied over the years. Oxytocin neurons are activated in response to various types of stressful stimuli (Ludwig 1998;Neumann 2002), and recent work has suggested the presence of an oxytocin-mediated, parasympathetically driven "anti-stress" system (Uvnas-Moberg 1997).…”

Release of Oxytocin in the Rat Central Amygdala Modulates Stress-Coping Behavior and the Release of Excitatory Amino Acids

“…There is, however, accumulating evidence that OXT released within various brain regions is a regulator of emotionality and physiological stress responses not only in the female rat (Windle et al, 1997(Windle et al, , 2004Neumann et al, 2000aNeumann et al, , 2001Lightman et al, 2001) but also in males as it plays an important role in cardiovascular (Callahan et al, 1989) and neuroendocrine (Neumann et al, 2000b) responses to an acute stressor. Stress exposure triggers not only OXT secretion into blood (Lang et al, 1983;Kasting, 1988;Wotjak et al, 1998) but also within the brain as reflected by increased OXT concentrations in the cerebrospinal fluid (Iványi et al, 1991) and extracellular space of several brain regions (for review, see Landgraf and Neumann, 2004).…”