Central cardiovascular effects of AVP and AVP analogs with V1, V2 and ‘V3’ agonistic or anatagonistic properties in conscious dog

Noszczyk, Bartłomiej; Lon, S.; Szczepañska‐Sadowska, Ewa

doi:10.1016/0006-8993(93)91224-g

Cited by 31 publications

(11 citation statements)

References 27 publications

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“…Centrally projecting vasopressinergic neurons innervate several groups of neurons engaged in cardiovascular control such as the NTS, RVLM, DVMNc, PBN, amygdala, BNST, periaqueductal gray matter, striatum, and the prefrontal cortex [ 212 •, 218 •, 219 •, 295 •]. There is significant evidence that centrally acting AVP may evoke both pressor and hypotensive responses [ 137 •, 145 •, 296 •, 297 •] and that the final effect depends on the stimulation of specific groups of vasopressinergic fibers innervating special sets of cardiovascular neurons and activated by specific stimuli.…”

Section: Vasopressinmentioning

confidence: 99%

Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders

2018

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Purpose of ReviewIn many instances, the renin-angiotensin system (RAS) and the vasopressinergic system (VPS) are jointly activated by the same stimuli and engaged in the regulation of the same processes.Recent FindingsAngiotensin II (Ang II) and arginine vasopressin (AVP), which are the main active compounds of the RAS and the VPS, interact at several levels. Firstly, Ang II, acting on AT1 receptors (AT1R), plays a significant role in the release of AVP from vasopressinergic neurons and AVP, stimulating V1a receptors (V1aR), regulates the release of renin in the kidney. Secondly, Ang II and AVP, acting on AT1R and V1aR, respectively, exert vasoconstriction, increase cardiac contractility, stimulate the sympathoadrenal system, and elevate blood pressure. At the same time, they act antagonistically in the regulation of blood pressure by baroreflex. Thirdly, the cooperative action of Ang II acting on AT1R and AVP stimulating both V1aR and V2 receptors in the kidney is necessary for the appropriate regulation of renal blood flow and the efficient resorption of sodium and water. Furthermore, both peptides enhance the release of aldosterone and potentiate its action in the renal tubules.SummaryIn this review, we (1) point attention to the role of the cooperative action of Ang II and AVP for the regulation of blood pressure and the water-electrolyte balance under physiological conditions, (2) present the subcellular mechanisms underlying interactions of these two peptides, and (3) provide evidence that dysregulation of the cooperative action of Ang II and AVP significantly contributes to the development of disturbances in the regulation of blood pressure and the water-electrolyte balance in cardiovascular diseases.

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Section: Vasopressinmentioning

confidence: 99%

Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders

2018

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“…9,10,53,54 These biologic effects are mediated by V 1 , V 2 , and V 3 (V 1b ) receptors that show specific tissue distribution, allowing design of selective targeting approaches. 55‐58 V 1 receptors mediate the vascular effects of AVP. 55,58 V 2 receptors mediate renal effects, while V 3 (V 1b ) receptors are involved in the regulation of ACTH secretion.…”

Section: Physiologic Role Of Arginine Vasopressinmentioning

confidence: 99%

“…55‐58 V 1 receptors mediate the vascular effects of AVP. 55,58 V 2 receptors mediate renal effects, while V 3 (V 1b ) receptors are involved in the regulation of ACTH secretion. 58…”

Section: Physiologic Role Of Arginine Vasopressinmentioning

confidence: 99%

Perturbations of Arginine Vasopressin Secretion during Inflammatory Stress: Pathophysiologic Implications

Chikanza¹,

Petrou

Chrousos

2000

Annals of the New York Academy of Sciences

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A BSTRACT : Pro-inflammatory cytokines, such as interleukin-1 ␤ (IL-1 ␤ ) , interleukin-6 (IL-6), and tumor necrosis factor-␣ (TNF ␣ ), released from inflammatory foci, can activate the hypothalamus to produce corticotrophinreleasing hormone (CRH) and arginine vasopressin (AVP). These hypothalamic peptides in synergy increase ACTH production by the pituitary gland and hence corticosteroid (CS) secretion by the adrenal cortices. CS dampens inflammation. The pituitary also produces prolactin (PRL), which is proinflammatory, and macrophage inhibitory factor (MIF), which by counteracting the anti-inflammatory and immunosuppressive effects of CS, is pro-inflammatory. Lewis rats develop a variety of induced-autoimmune inflammatory conditions, such as streptococcal cell wall arthritis, whereas the histocompatible F344 Fisher rats are resistant to this condition. Lewis rats have a defective hypothalamic-pituitary adrenal (HPA) response to a variety of hypothalamic stimuli, but have augmented systemic secretion of AVP. Patients with rheumatoid arthritis (RA) have deficient CS with exaggerated PRL responses to inflammatory stimuli. Within inflammatory foci, CRH is pro-inflammatory. AVP, which augments autologous mixed lymphocyte reactions, can replace the IL-2 requirement for ␥ IFN production by T cells via V 1a receptors, and potentiates primary antibody responses, is also pro-inflammatory. Lewis rats have significantly high plasma levels, hypothalamic content, and in vitro release of AVP in comparison to the inflammatory disease-resistant Fischer rats. Immunoneutralization of AVP attenuates inflammatory responses. In Sprague-Dawley rats, AVP potentiates PRL secretion. Preliminary studies in patients with RA have shown that the circulating levels of AVP are significantly increased, which might be a compensatory response to low CS levels or a result of elevated levels of IL-6 in these patients but could nevertheless contribute to rheumatoid inflammation. A similar observation has been made in patients with ankylosing spondylitis.

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“…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).…”

Section: Introductionmentioning

confidence: 97%

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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Central cardiovascular effects of AVP and AVP analogs with V1, V2 and ‘V3’ agonistic or anatagonistic properties in conscious dog

Cited by 31 publications

References 27 publications

Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders

Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders

Perturbations of Arginine Vasopressin Secretion during Inflammatory Stress: Pathophysiologic Implications

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

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