Atrial natriuretic factor inhibits norepinephrine biosynthesis and turnover in the rat hypothalamus

Vatta, Marcelo S.; Rodrı́guez-Fermepı́n, Martı́n; Durante, Gabriela Dalcin; Bianciotti, Liliana G.; Fernández, Belisario E.

doi:10.1016/s0167-0115(99)00083-x

Cited by 23 publications

(4 citation statements)

References 32 publications

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“…20 Vatta et al 21 demonstrated that ANP plays a role in the modulation of norepinephrine (NE) metabolism in the rat hypothalamus and adrenal medulla, affecting storage, release, and uptake of NE. They concluded that ANP acts as an inhibitor of noradrenergic neurotransmission.…”

Section: Alternative Explanations For Increased Vascular Volume?mentioning

confidence: 99%

Atrial Natriuretic Peptide Regulates Regional Vascular Volume and Venous Tone in Humans

Schmitt

Broadley

Nightingale

et al. 2003

ATVB

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Objective-To date, the contribution of basal atrial natriuretic peptide (ANP) levels to resting vascular function in humans is unknown. In the present study we sought to investigate the role of ANP in regulating regional vascular volume and venous tone in healthy subjects. Methods and Results-We used radionuclide plethysmography to examine the effects of ANP and the ANP-receptor antagonist A71915 on forearm vascular volume. Creating pressure/volume relations, we determined changes in vascular volume, compliance, and tone. Performing dose-ranging studies, we additionally assessed the potency and specificity of A71915 in the forearm resistance vasculature. Equilibrium blood pool scintigraphy was then used to assess the effects of systemic administration of A71915 on regional intestinal vascular volume. Infusion of ANP increased forearm vascular volume in a dose-dependent manner (maximum 20%; PϽ0.001), exerting a maximum venodilating effect at plasma levels similar to that seen in heart failure. A71915 increased venous tone, thereby decreasing vascular volume by 9.6Ϯ1.1%, PϽ0.001 (forearm), and 2.6Ϯ0.5%, Pϭ0.01 (intestinal beds). At an infusion ratio of 50:1, A71915 almost completely abolished the effects of ANP on forearm blood flow. A trial natriuretic peptide (ANP) plays an important role in cardiovascular control, being a major determinant of sodium homeostasis, plasma volume, and blood pressure (BP). Although intraarterial infusion of ANP produces vasorelaxation of resistance vessels, 1,2 this may not be the underlying mechanism of the fall in BP that accompanies systemic ANP infusion. Animal studies 3,4 have shown that the fall in BP and cardiac output are almost invariably associated with a fall in central venous pressure (CVP) and, in fact, an increase in total peripheral resistance. Indeed, Groban et al 5 demonstrated in humans that low-dose systemic infusion of ANP reduced CVP without affecting BP. It is now generally accepted that the fall in cardiac output and BP after systemic infusion of ANP is a consequence of reduced preload. 6 Possible mechanisms include volume contraction as a result of diuresis, increased capillary filtration, 7 and direct venodilation, even though no venorelaxant effects of ANP were observed in dorsal hand veins 2 and saphenous veins. 8 Given that atrial stretch is the principal stimulus for ANP release, 9 the apparent lack of a direct effect on venous tone in humans seems counterintuitive. In addition, the contribution of basal levels of ANP to human resting vascular function is unknown, but acceptance of ANP as a physiologically important vasoactive hormone in health clearly depends on its contribution being significant. Conclusions-ANPWe hypothesized that, despite its lack of action on conduit veins, ANP may act as a venodilator on the small veins and venules that constitute most of the capacitance vasculature. To study the effect of ANP on vascular function in general and venous tone in particular, we performed 4 experiments. In experiment 1, we evaluated the effect of incre...

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Section: Alternative Explanations For Increased Vascular Volume?mentioning

confidence: 99%

Atrial Natriuretic Peptide Regulates Regional Vascular Volume and Venous Tone in Humans

Schmitt

Broadley

Nightingale

et al. 2003

ATVB

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“…This could be achieved through inhibition of the sympathetic fibers to the hypothalamic PVN, and their projections to the locus coeruleus and brain stem sympathetic nuclei. In support of this hypothesis, ANP inhibits NE biosynthesis and release from hypothalamus in vitro [Vatta et al, 1999].…”

Section: The Role Of Natriuretic Peptides In Mood Disordersmentioning

confidence: 77%

Angiotensin II AT₁ receptor antagonists inhibit the angiotensin‐CRF‐AVP axis and are potentially useful for the treatment of stress‐related and mood disorders

Saavedra

Pavel

2005

Drug Development Research

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The corticotropin-releasing factor (CRF), arginine-vasopressin (AVP), atrial natriuretic peptide (ANP), and Angiotensin II (Ang II) interact, regulating the central sympathetic system, the hypothalamic-pituitary-adrenal (HPA) axis, and the central behavioral mechanisms involved in the response to stress and the development of mood disorders. Non-peptidic, orally active AVP V 1 , V 3 , or CRF 1 receptor antagonists reduce anxiety in animals. ANP is anxiolytic when administered to rodents and humans with anxiety disorders. These compounds are being developed for the therapy of anxiety and depression, but their clinical efficacy has not yet been established.Brain Ang II, a physiological ANP antagonist, promotes CRF and AVP release and stimulates the peripheral and central sympathetic systems. The degree of Ang II AT 1 receptor stimulation determines the response to stress. An orally active, non-peptidic Ang II AT 1 receptor antagonist blocks CRF and AVP release during stress, prevents the sympathoadrenal and hormonal stress reaction, the cortical CRF 1 and benzodiazepine receptor alterations, facilitates the effects of ANP, prevents stress-induced gastric ulcerations, and is anxiolytic in rodents. CRF, AVP, ANP, and the sympathetic system are intimately linked parts of a fundamental regulatory mechanism controlled by the brain Ang II system through AT 1 receptor stimulation, and should be studied together. Selective, safe antagonists of Ang II AT 1 receptors, with central effects after oral administration, have been actively used for the treatment of hypertension and should be considered also as potential anti-stress, anti-anxiety, and antidepressant compounds with properties similar or superior to the CRF and AVP antagonists or the ANP agonists under development. Drug Dev. Res. 65:237-269, 2005.

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“…Marin-Grez et al and Webb et al have reported that part of ANP inhibitory effects on sodium and water reabsorption is mediated by dopaminergic mechanisms, since haloperidol and the D 1 receptor antagonist SCH 23390 partially blocked a significant percentage of the natriuretic and diuretic effects of ANP [53, 55]. In a similar fashion, ANP can modulate the metabolism of another catecholamine like noradrenaline, since it has been demonstrated that ANP increases norepinephrine uptake and its endogenous content and decreases its release, synthesis, and turnover and tyrosine hydroxylase activity at the hypothalamic presynaptic nerve ending level [56, 57]. The natriuretic peptides also regulate norepinephrine metabolism in the adrenal medulla [58].…”

Section: Regulation Of Renal Dopamine System By the Atrial Natriurmentioning

confidence: 99%

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

Choi

Mikusic

Kouyoumdzian

et al. 2014

BioMed Research International

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Sodium metabolism by the kidney is accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Renal dopamine plays a central role in this interactive network. The natriuretic hormones, such as the atrial natriuretic peptide, mediate some of their effects by affecting the renal dopaminergic system. Renal dopaminergic tonus can be modulated at different steps of dopamine metabolism (synthesis, uptake, release, catabolism, and receptor sensitization) which can be regulated by the atrial natriuretic peptide. At tubular level, dopamine and atrial natriuretic peptide act together in a concerted manner to promote sodium excretion, especially through the overinhibition of Na+, K+-ATPase activity. In this way, different pathological scenarios where renal sodium excretion is dysregulated, as in nephrotic syndrome or hypertension, are associated with impaired action of renal dopamine and/or atrial natriuretic peptide, or as a result of impaired interaction between these two natriuretic systems. The aim of this review is to update and comment on the most recent evidences demonstrating how the renal dopaminergic system interacts with atrial natriuretic peptide to control renal physiology and blood pressure through different regulatory pathways.

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Atrial natriuretic factor inhibits norepinephrine biosynthesis and turnover in the rat hypothalamus

Cited by 23 publications

References 32 publications

Atrial Natriuretic Peptide Regulates Regional Vascular Volume and Venous Tone in Humans

Atrial Natriuretic Peptide Regulates Regional Vascular Volume and Venous Tone in Humans

Angiotensin II AT₁ receptor antagonists inhibit the angiotensin‐CRF‐AVP axis and are potentially useful for the treatment of stress‐related and mood disorders

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

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Atrial natriuretic factor inhibits norepinephrine biosynthesis and turnover in the rat hypothalamus

Cited by 23 publications

References 32 publications

Atrial Natriuretic Peptide Regulates Regional Vascular Volume and Venous Tone in Humans

Atrial Natriuretic Peptide Regulates Regional Vascular Volume and Venous Tone in Humans

Angiotensin II AT1 receptor antagonists inhibit the angiotensin‐CRF‐AVP axis and are potentially useful for the treatment of stress‐related and mood disorders

Atrial Natriuretic Peptide and Renal Dopaminergic System: A Positive Friendly Relationship?

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Angiotensin II AT₁ receptor antagonists inhibit the angiotensin‐CRF‐AVP axis and are potentially useful for the treatment of stress‐related and mood disorders