Chronic regulation of arterial blood pressure in ANP transgenic and knockout mice: Role of cardiovascular sympathetic tone

Melo, Luis G.; Veress, A. T.; Ackermann, Uwe; Steinhelper, Mark E.; Pang, Stephen C.; Tse, Yat; Sonnenberg, H.

doi:10.1016/s0008-6363(99)00104-2

Cited by 49 publications

(49 citation statements)

References 45 publications

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“…In both adrenal gland and SNS nerve terminals, NP reduce CA production via a cGMP-dependent activation of tyrosine hydroxylase, the rate-limiting enzyme in CA synthesis (Holtz et al, 1987). This effect is corroborated by the high circulating CA levels found in genetically modified mice with ANP gene disruption (Melo et al, 1999). On the other hand, the effects of adrenergic stimulation on mammalian cardiac NP release are still in part unknown because of confusing results mainly derived from clinical studies carried out in the presence of different pathological conditions and/or therapies.…”

Section: Np Ca and The Stressed Heartmentioning

confidence: 76%

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Tota

Cerra

Gattuso

2010

Journal of Experimental Biology

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Summary In the past 50 years, extensive evidence has shown the ability of vertebrate cardiac non-neuronal cells to synthesize and release catecholamines (CA). This formed the mindset behind the search for the intrinsic endocrine heart properties, culminating in 1981 with the discovery of the natriuretic peptides (NP). CA and NP, co-existing in the endocrine secretion granules and acting as major cardiovascular regulators in health and disease, have become of great biomedical relevance for their potent diagnostic and therapeutic use. The concept of the endocrine heart was later enriched by the identification of a growing number of cardiac hormonal substances involved in organ modulation under normal and stress-induced conditions. Recently, chromogranin A (CgA), a major constituent of the secretory granules, and its derived cardio-suppressive and antiadrenergic peptides, vasostatin-1 and catestatin, were shown as new players in this framework, functioning as cardiac counter-regulators in ‘zero steady-state error’ homeostasis, particularly under intense excitatory stimuli, e.g. CA-induced myocardial stress. Here, we present evidence for the hypothesis that is gaining support, particularly among human cardiologists. The actions of CA, NP and CgA, we argue, may be viewed as a hallmark of the cardiac capacity to organize ‘whip-brake’ connection-integration processes in spatio-temporal networks. The involvement of the nitric oxide synthase (NOS)/nitric oxide (NO) system in this configuration is discussed. The use of fish and amphibian paradigms will illustrate the ways that incipient endocrine-humoral agents have evolved as components of cardiac molecular loops and important intermediates during evolutionary transitions, or in a distinct phylogenetic lineage, or under stress challenges. This may help to grasp the old evolutionary roots of these intracardiac endocrine/paracrine networks and how they have evolved from relatively less complicated designs. The latter can also be used as an intellectual tool to disentangle the experimental complexity of the mammalian and human endocrine hearts, suggesting future investigational avenues.

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Section: Np Ca and The Stressed Heartmentioning

confidence: 76%

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Tota

Cerra

Gattuso

2010

Journal of Experimental Biology

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“…Vasodilatation 68 Modulation of endothelial permeability 69 Central Nervous System Effects Modulation of sympathetic activity 70,71 Inhibition of arginine vasopressin secretion 47,72 Diminished salt appetite and water drinking 47,60 Effects on blood pressure/volume-regulating regions in the brain 47,60 than do ANP-deficient mice. Whereas BNP-deficient mice do not have hypertension or cardiac hypertrophy, they are susceptible to cardiac fibrosis.…”

Section: Vascular Effectsmentioning

confidence: 99%

“…47,60 -72 In particular, the renal [63][64][65][66] and sympatholytic actions of ANP 70,71 probably have a major role in the hypotensive actions of the peptide. In contrast, the relevance of the direct vasodilating ANP effect is controversial, because very variable GC-A levels are expressed in different vascular beds.…”

Section: Endocrine Actions Of the Anp/gc-a System Cooperate In Acute mentioning

confidence: 99%

Structure, Regulation, and Function of Mammalian Membrane Guanylyl Cyclase Receptors, With a Focus on Guanylyl Cyclase-A

Kühn

2003

Circulation Research

240

161

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Abstract-Besides soluble guanylyl cyclase (GC), the receptor for NO, there are at least seven plasma membrane enzymes that synthesize the second-messenger cGMP. All membrane GCs (GC-A through GC-G) share a basic topology, which consists of an extracellular ligand binding domain, a short transmembrane region, and an intracellular domain that contains the catalytic (GC) region. Although the presence of the extracellular domain suggests that all these enzymes function as receptors, specific ligands have been identified for only three of them (GC-A through GC-C). GC-A mediates the endocrine effects of atrial and B-type natriuretic peptides regulating arterial blood pressure and volume homeostasis and also local antihypertrophic actions in the heart. GC-B is a specific receptor for C-type natriuretic peptide, having more of a paracrine function in vascular regeneration and endochondral ossification. GC-C mediates the effects of guanylin and uroguanylin on intestinal electrolyte and water transport and on epithelial cell growth and differentiation. GC-E and GC-F are colocalized within the same photoreceptor cells of the retina and have an important role in phototransduction. Finally, the functions of GC-D (located in the olfactory neuroepithelium) and GC-G (expressed in highest amounts in lung, intestine, and skeletal muscle) are completely unknown. This review discusses the structure and functions of membrane GCs, with special emphasis on the physiological endocrine and cardiac functions of GC-A, the regulation of hormone-dependent GC-A activity, and the relevance of alterations of the atrial natriuretic peptide/GC-A system to cardiovascular diseases. (Circ Res. 2003;93:700-709.)

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“…The diuretic, natriuretic and vasodilator actions of natriuretic peptides are mediated by cell membrane natriuretic peptide receptor A (NPR-A) and NPR-B, through activation of guanylyl cyclase/cGMP, and NPR-C (clearance receptor), through inhibition of adenylyl cyclase/cAMP. The important role of ANP on chronic blood pressure regulation has been shown in a transgenic mouse model overexpressing ANP (26,27), where elevated plasma ANP was associated with significant blood pressure reduction, whereas NPR-A knockout mice are hypertensive. The knockout studies revealed that the chronic hypotensive effect of ANP is mediated by attenuation of cardiovascular sympathetic tone (27).…”

Section: Imidazoline and Natriuretic Peptidesmentioning

confidence: 99%

“…The important role of ANP on chronic blood pressure regulation has been shown in a transgenic mouse model overexpressing ANP (26,27), where elevated plasma ANP was associated with significant blood pressure reduction, whereas NPR-A knockout mice are hypertensive. The knockout studies revealed that the chronic hypotensive effect of ANP is mediated by attenuation of cardiovascular sympathetic tone (27). Independent of their role in blood pressure control, natriuretic peptides have antiinflammatory effects, and exert direct antihypertrophic and anti-fibrotic actions on the heart.…”

Section: Imidazoline and Natriuretic Peptidesmentioning

confidence: 99%

Imidazoline receptors in the heart: a novel target and a novel mechanism of action that involves atrial natriuretic peptides

Mukaddam‐Daher

Gutkowska

2004

Braz J Med Biol Res

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Chronic stimulation of sympathetic nervous activity contributes to the development and maintenance of hypertension, leading to left ventricular hypertrophy (LVH), arrhythmias and cardiac death. Moxonidine, an imidazoline antihypertensive compound that preferentially activates imidazoline receptors in brainstem rostroventrolateral medulla, suppresses sympathetic activation and reverses LVH. We have identified imidazoline receptors in the heart atria and ventricles, and shown that atrial I 1 -receptors are up-regulated in spontaneously hypertensive rats (SHR), and ventricular I 1 -receptors are up-regulated in hamster and human heart failure. Furthermore, cardiac I 1 -receptor binding decreased after chronic in vivo exposure to moxonidine. These studies implied that cardiac I 1 -receptors are involved in cardiovascular regulation. The presence of I 1 -receptors in the heart, the primary site of production of natriuretic peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), cardiac hormones implicated in blood pressure control and cardioprotection, led us to propose that ANP may be involved in the actions of moxonidine. In fact, acute iv administration of moxonidine (50 to 150 µg/rat) dose-dependently decreased blood pressure, stimulated diuresis and natriuresis and increased plasma ANP and its second messenger, cGMP. Chronic SHR treatment with moxonidine (0, 60 and 120 µg kg -1 h -1 , sc for 4 weeks) dosedependently decreased blood pressure, resulted in reversal of LVH and decreased ventricular interleukin 1ß concentration after 4 weeks of treatment. These effects were associated with a further increase in already elevated ANP and BNP synthesis and release (after 1 week), and normalization by 4 weeks. In conclusion, cardiac imidazoline receptors and natriuretic peptides may be involved in the acute and chronic effects of moxonidine. Correspondence S. Mukaddam-Daher

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Chronic regulation of arterial blood pressure in ANP transgenic and knockout mice: Role of cardiovascular sympathetic tone

Cited by 49 publications

References 45 publications

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Catecholamines, cardiac natriuretic peptides and chromogranin A: evolution and physiopathology of a ‘whip-brake’ system of the endocrine heart

Structure, Regulation, and Function of Mammalian Membrane Guanylyl Cyclase Receptors, With a Focus on Guanylyl Cyclase-A

Imidazoline receptors in the heart: a novel target and a novel mechanism of action that involves atrial natriuretic peptides

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