Atrial natriuretic peptide receptor

Asu ]-P-ANP(7-28) ([L-a-aminosuberic acid l-P-AMP7.28) is reported to be an ATRIAL NATRIURETIC PEPTIDE receptor ANTAGONIST selective for the type A (ANP ) receptor subtype. 

ATRIAL NATRIURETIC PEPTIDE RECEPTOR AGONISTS include ANP itself (also called atrial natriuretic factor (ANF), or atrlopeptin), a peptide made up of 28 amino acids and is contained in secretory granules in heart atrial cells. ANP is released in response to stretch in the atria, as occurs with increased central venous pressure, thus signalling volume overload in the circulation. The peptide has an effect on the kidney leading to increased Na and water excretion, vasodilation, increased vascular permeability and modified release of a number of other hormones and neurotransmitters. There are at least three related endogenous peptides ANP (atrial natriuretic peptide),... 

ATRIAL NATRIURETIC PEPTIDE RECEPTOR ANTAGONISTS act at receptors recognizing atrial... 

C-type natriuretic peptide (CNP) the newest member of the natriuretic peptide family, was first isolated from porcine brain, and later found in other mammals and nonmammals. It is processed from a pre-pro-CNP molecule, which gives rise to CNP-22 and its N-terminally elongated form. CNP-53. The CNP s share considerable sequence homology with atrial NATRIURETIC PEPTIDES (ANP) and brain natriuretic peptides (BNP). CNP s are atrial NATRIURETIC PEPTIDE RECEPTOR AGONISTS but are more active at the type-B subtype, whereas ANP s are more active at the type-A subtype. 

C. Clinical Role ANP has been studied for possible use in the treatment of congestive heart failure, but results have been mixed. BNP has showed some benefit in small studies in patients with heart failure. At present there are no clinically important products that act as agonists or antagonists at atrial natriuretic peptide receptors. 

Chinkers M, Garbers DL, Chang MS, et al. A membrane form of guanylate cyclase is an atrial natriuretic peptide receptor. Nature 1989 338 78-83. 

Wang Z-Z, Hirose S, Dinger B, Fidone S, Stensaas LJ. Localization of atrial natriuretic peptide receptors in the carotid body. Soc Neurosci Abstr 1991 17 118. 

Urodilatin is a peptide similar to atrial natriuretic peptide, which is produced in the distal tubule of the kidney and promotes sodium excretion and diuresis by acting on receptors localized on the luminal site of the collecting duct of the nephron. 

The vascular endothelium produces a number of substances that are released basally into the blood vessel wall to alter vascular smooth muscle tone. One such substance is endothelin (ET-1). Endothelin exerts its effects throughout the body, causing vasoconstriction as well as positive inotropic and chronotropic effects on the heart. The resulting increases in TPR and CO contribute to an increase in MAP. Synthesis of endothelin appears to be enhanced by many stimuli, including Ag II, vasopressin, and the mechanical stress of blood flow on the endothelium. Synthesis is inhibited by vasodilator substances such as prostacyclin, nitric oxide, and atrial natriuretic peptide. There is evidence that endothelin is involved with the pathophysiology of many cardiovascular diseases, including hypertension, heart failure, and myocardial infarction. Endothelin receptor antagonists are currently available for research use only. 

There are seven membrane forms of GC, designated GC-A to GC-G [33], Two forms, GC-A and GC-B (Mr = 120kDa), serve as receptors for atrial natriuretic peptide (ANP) and related peptides. ANP is a 28-amino-acid peptide isolated originally from cardiac atria as an important factor in the regulation of sodium excretion and blood pressure. GC-A binds ANP, as well as brain natriuretic peptide (BNP), and is located in vascular tissue and kidney. 

Atrial natriuretic peptide binds to the GPCR receptor. 

Whereas several peptides besides AVP are known to act synergistically with CRH, the only peptide candidate in humans that inhibits the HPA system at all regulatory levels of the system seems to be atrial natriuretic peptide (ANP). ANP has been shown to inhibit the stimulated release of CRH and ACTH in vitro and in vivo. This could be observed in humans as well, where ANP inhibits the CRH-induced ACTH (Keller et al. 1992), prolactin (Wiedemann et al. 1995), and cortisol secretion (StrOhle et al. 1998). ANP is not only synthesized by atrial myocytes (deBold et al. 1985) and released into the circulation, but is also found in neurons of different brain regions (Tanala et al. 1984) where specific receptors have been found. ANP receptors and immunoreactivity have been found in periventricular and paraventricular hypothalamic nuclei, the LC, and the central nucleus of the amygdala. 

StrOhle A, Pasini A, Romeo E, Hermann B, Spalletta G, di Michele F, Holsboer F, Rupprecht R (2000) Fluoxetine decreases concentrations of 3a,5a-tetrahydrodeoxycorticosterone (3a,5a-THDOC) in major depression. J Psychiatr Res 34 183-186 StrOhle A, Kellner M, Holsboer F, Wiedemann K (2001) Anxiolytic activity of atrial natriuretic peptide in patients with panic disorder. Am J Psychiatry 158 1514-1516 StrOhle A, Romeo E, di Michele F, Pasini A, Yassouridis A, Holsboer F, Rupprecht R (2002) GABAA receptor modulatory neuroactive steroid composition in panic disorder and during paroxetine treatment. Am J Psychiatry 159 145-147 StrOhle A, Romeo E, di Michele F, Pasini A, Hermann B, Gajewsky G, Holsboer F, Rupprecht F (2003) Induced panic attacks shift GABAA receptor modulatory neuroactive steroid composition. Arch Gen Psychiatry 60 161-168 Szapiro G, Vianna MRM, McGaugh JL, Medina JH, Izquierdo I (2003) The role of NMDA glutamate receptors, PKA, MAPK, and CAMKII in the hippocampus in extinction of conditioned fear. Hippocampus 13 53-58... 

Verspohl, E. J., Kuhn, M., and Ammon, H. P. T. (1988). RlNm5F (Rat insulinoma) cells possess receptors for atrial natriuretic peptide (ANP) and a functioning cGMP system Harm. Metab. Res. 20, 770-771. 

Contractile elements of the podocyte foot processes, which may influence the hydraulic permeability of the glomerular capillary wall, may be regulated via vasoactive hormones. Receptors for some vasoactive hormones, for example, en-dothelin (R4), atrial natriuretic peptide (S9), nitric oxide (K22), and angiotensin n (Yl), have been described on the podocyte surface. 

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