Enhanced involvement of brain vasopressin V1 receptors in cardiovascular responses to stress in rats with myocardial infarction

Abstract

Stress is one of the factors provoking cardiovascular complications. The purpose of the study was to explore the role of vasopressin (VP) in central control of arterial blood pressure and heart rate under resting conditions and during stimulation by an alarming stress (air jet stress) in myocardial infarct-induced cardiac failure. Six groups of male Sprague Dawley (SD) rats were subjected either to sham surgery (sham rats) or to ligation of a left coronary artery (infarcted rats). After 5 weeks both infarcted and sham rats were subjected either to intracerebroventricular infusion of artificial cerebrospinal fluid (aCSF) (sham aCSF and infarcted aCSF), [Arg8]-VP (sham VP and infarcted VP) or VP V1a receptor antagonist (d(CH2)5[Tyr(Me)2Ala-]VP, sham V1ANT and infarcted V1ANT). Air jet stress elicited significantly greater increases in mean arterial blood pressure (MABP) and heart rate in the infarcted aCSF than in the sham aCSF rats. Intracerebroventricular infusion of V1ANT significantly reduced resting MABP and MABP and heart rate increases in response to stress in the infarcted but not in the sham rats. Intracerebroventricular infusion of VP elicited a significant increase in resting MABP in the infarcted VP but not in the sham VP rats. The results provide evidence for enhanced engagement of the brain V1 VP receptors in regulation of resting MABP and in generation of exaggerated cardiovascular responses to air jet stress during the post-infarct state.

Differential sensitisation to central cardiovascular effects of angiotensin II in rats with a myocardial infarct: Relevance to stress and interaction with vasopressin

“…administration of an AT1 or V1a antagonist (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999). Accordingly, it was concluded that myocardial infarction results in an enhanced activation of those central AT1 and V1a receptors which participate in cardiovascular regulation under resting conditions and during stress (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999). In our previous studies, we described sensitisation to the central pressor action of VP, and an interaction between AT1 and V1a receptors in central cardiovascular control in infarcted rats (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005).…”

“…The infarct size was determined by planimetry as described by Leenen et al (1999), with some minor modifications , and expressed as a percentage of the total left ventricle surface. In addition, the heart was examined histologically to confirm the presence of an infarct scar according to the procedure described previously (Cudnoch-Jędrzejewska et al 2005;Dobruch et al 2005). To verify whether the i.c.v.…”

“…In addition, increasing evidence indicates that ANG II may be involved in resetting central cardiovascular control in various models of hypertension, and in post-infarct cardiac failure (Cudnoch-Jedrzejewska et al 2007; Kagiyama et al 2001;Kubo et al 2000;Leenen et al 1999;Szczepanska-Sadowska et al 1998; Wang and Ma 2000;Zhang et al 1999;Zhu et al 2004;Zucker et al 2004). With regard to post-infarct cardiac failure, it has been established that a blockade of central AT1 receptors for ANG II and V1a receptors for VP significantly reduces MABP and renal sympathetic nerve activity in rats with a myocardial infarct while the same procedure was not effective in shamoperated rats (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Leenen et al 1999;Zhang et al 1999). In comparison with sham-ligated (SL) rats the infarcted rats manifested also exaggerated cardiovascular responses to the alarming stressor that could be normalised by the intracerebroventricular (i.c.v.)…”

“…In comparison with sham-ligated (SL) rats the infarcted rats manifested also exaggerated cardiovascular responses to the alarming stressor that could be normalised by the intracerebroventricular (i.c.v.) administration of an AT1 or V1a antagonist (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999). Accordingly, it was concluded that myocardial infarction results in an enhanced activation of those central AT1 and V1a receptors which participate in cardiovascular regulation under resting conditions and during stress (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999).…”

“…Accordingly, it was concluded that myocardial infarction results in an enhanced activation of those central AT1 and V1a receptors which participate in cardiovascular regulation under resting conditions and during stress (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999). In our previous studies, we described sensitisation to the central pressor action of VP, and an interaction between AT1 and V1a receptors in central cardiovascular control in infarcted rats (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005). Thus far, cardiovascular studies conducted on infarcted rats have focused only on the role of the central AT1 receptors (CudnochJedrzejewska et al 2007;Zhang et al 1999).…”