Interaction of AT1 receptors and V1a receptors-mediated effects in the central cardiovascular control during the post-infarct state

Cudnoch-Jędrzejewska, Agnieszka; Dobruch, Jakub; Puchalska, Liana; Szczepañska‐Sadowska, Ewa

doi:10.1016/j.regpep.2007.01.010

Cited by 24 publications

(35 citation statements)

References 49 publications

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“…The present results confirm other reports in which it was demonstrated that an alarming stressor elicits greater pressor and tachycardic responses in infarcted than in SL rats (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999). Previous studies provided also evidence that differences in the pressor and tachycardic responses to the alarming stressor between infarcted and SL rats can be abolished by blockade of central AT1 and V1a receptors (Cudnoch-Jedrzejewska et al 2007;Dobruch et al 2005;Zhang et al 1999).…”

Section: Effect Of Ang II On Cardiovascular Responsiveness To the Alasupporting

confidence: 92%

“…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).…”

Section: Introductionmentioning

confidence: 95%

“…There is a general consensus that central administration of these peptides heightens the sympathetic drive and exerts significant pressor effects (DiBona 1999;Ganten et al 1985;Janiak et al 1989;Łoń et al 1996;Noszczyk et al 1993;Paczwa et al 1997). 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).…”

Section: Introductionmentioning

confidence: 99%

“…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).…”

Section: Introductionmentioning

confidence: 99%

“…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).…”

Section: Introductionmentioning

confidence: 99%

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

Cudnoch‐Jędrzejewska

Szczepañska‐Sadowska

Dobruch

et al. 2008

Stress

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The purpose of the present study was to elucidate if rats with myocardial infarction manifest altered responsiveness to central cardiovascular effects of low doses of angiotensin II (ANG II), and if ANG II and vasopressin (VP) cooperate in the central regulation of cardiovascular functions at rest and during stress. Conscious Sprague-Dawley rats with myocardial infarction induced by left coronary artery ligation, or sham-ligated (SL) controls were infused intracerebroventricularly with artificial cerebrospinal fluid (aCSF), ANG II, ANG II + VP or ANG II + V1a receptor antagonist (V1ANT) 4 weeks after cardiac surgery. In the infarcted but not in the SL rats, the resting mean arterial blood pressure (MABP) was significantly elevated by infusions of ANG II and ANG II + VP, while infusion of ANG II + V1ANT was not effective. During administration of aCSF, the pressor, and tachycardic responses to an air-jet stressor were significantly greater in the infarcted than in the SL rats. In the SL rats, the pressor responses to the stressor were significantly greater during infusions of ANG II, ANG II + VP and ANG II + V1ANT than during infusion of aCSF. The tachycardic response in the SL rats was enhanced only by the combined infusion of ANG II + VP. In the infarcted rats, the pressor and the tachycardic responses to the stressor were similar in all groups. It is concluded that: (1) under resting conditions the infarcted rats manifest sensitisation to the central pressor effect of ANG II and that this effect depends on concomitant stimulation of V1a VP receptors, (2) central ANG II may enhance the pressor response to an alarming stressor in the SL rats through an action which does not depend on the concomitant stimulation of V1a receptors, (3) the cooperative action of ANG II and VP is required for intensification of the tachycardic response to the alarming stressor in the SL rats and (4) exaggeration of the cardiovascular responses to the alarming stressor in the infarcted rats cannot be further augmented by an additional stimulation of central ANG II receptors or combined stimulation of ANG II and VP receptors.

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