Disease relevance of Atrial peptide

• OBJECTIVES: The aim of the present study was to examine the relation between the plasma levels of the atrial peptide N-terminal proatrial natriuretic factor (proANF) measured during the 1st 12 h after myocardial infarction and 1-year mortality [1].
• Renal atrial peptide receptors and natriuresis in two-kidney, one clip hypertension [2].
• In contrast, atrial peptide secretion in ventricular disease has received less attention, and our present understanding of the endocrine atria during ventricular dysfunction is still scarce [3].
• This study was designed to investigate whether an infusion of atrial peptide is capable of modulating the hormonal and hemodynamic responses elicited by acute hemorrhage [4].
• The role of atrial peptide in humans with chronic renal insufficiency is uncertain [5].

High impact information on Atrial peptide

• A linear relation was found between right atrial pressure and right atrial peptide concentration (r = 0.835, P less than 0.001) and between pulmonary wedge pressure and the systemic arterial peptide concentration (r = 0.866, P less than 0.001) [6].
• The fact that atrial peptide works to oppose the renin system at four points suggests that this new hormone could have a major complementary role in long-term regulation of blood pressure and electrolyte homeostasis [7].
• Atrial natriuretic peptide (ANP)(31-67), a portion of the atrial peptide prohormone, circulates in humans, and its plasma level varies with atrial pressure [8].
• The results of model experiments suggest that the binding of this atrial peptide to the target cell membrane is associated with the induction of beta-sheet structure and that it is this latter conformation that is predominant in the active form of the hormone [9].
• These results suggest that atrial peptide can pass from atrial granules into caveolae by transiently open pathways between the interiors of granules and caveolae [10].

Chemical compound and disease context of Atrial peptide

• Our data suggest that the refractoriness to the effect of atrial peptide may be due to the reduced receptor sites in aldosterone-producing adenoma cells [11].

Biological context of Atrial peptide

• Mesenteric blood flow was reduced significantly, and mesenteric vascular resistance was increased markedly in all three groups of rats during infusion of the atrial peptide [12].
• Dynamics of atrial peptide secretion in the coronary circulation of the conscious dog [13].
• To test this hypothesis, blood volume expansion and atrial peptide binding studies were performed in this model [2].
• Between clipped and nonclipped kidneys, the association constant (5.26 +/- 0.89 versus 5.17 +/- 0.64 x 10(9)/mol) and apparent binding site density (575 +/- 92 versus 500 +/- 74 fmol/mg protein) for atrial peptide binding in isolated glomeruli did not differ [2].
• The atrial peptide partially inhibited ACTH-stimulated cAMP formation (IC50, approximately 10(-8) M) and partially antagonized basal and ACTH-stimulated steroidogenesis [14].

Anatomical context of Atrial peptide

• The results are interpreted as suggesting the presence of a second pathway for externalization of atrial natriuretic peptide through caveolae in addition to the classic pathway for regulated atrial peptide secretion at noncaveolar plasmalemma [10].
• The antiarrhythmic peptide analog rotigaptide (ZP123) stimulates gap junction intercellular communication in human osteoblasts and prevents decrease in femoral trabecular bone strength in ovariectomized rats [15].
• Volume status influences atrial peptide-induced water conductivity changes in leopard frog mesenteric capillaries [16].
• The antiarrhythmic peptide rotigaptide (ZP123) increases gap junction intercellular communication in cardiac myocytes and HeLa cells expressing connexin 43 [17].
• Body fluids and plasma atrial peptide after its chronic infusion in hypertensive rats [18].

Associations of Atrial peptide with other chemical compounds

• It has been suggested that renal disease is characterized by the presence of resistance to the natriuretic effects of atrial peptide (ANP) [19].
• The role of the vascular endothelium in atrial peptide-induced relaxation was examined in the presence of indomethacin and propranolol by removal of the endothelium in one of a pair of arterial segments [20].
• The modulation of baroreflexes by ANP seems to be related, at least in part, to the interaction of the atrial peptide with the effects of angiotensin II [21].
• Acute expansion of extracellular fluid volume before DOCA elicited significant increments in plasma EDLF and atrial peptide [22].
• The atrial peptide decreased mean blood pressure to a similar extent in rats pretreated with atropine (from 124 +/- 4.5 to 108 +/- 5.3 mm Hg, mean +/- S.E.M., P less than 0.05) and in the controls (from 123 +/- 3.8 to 105 +/- 3.8 mm Hg, P less than 0.05) [23].

Gene context of Atrial peptide

• Kallikrein activation of a high molecular weight atrial peptide [24].
• In frogs given free access to water and dry terrain the response to atrial peptide was similar to that observed in the DS group (Lp, AP-FA/Lp, BSA = 3.6 +/- 07; n = 23) [16].
• We studied changes in Cx43 phosphorylation during global ischemia in the absence and presence of the antiarrhythmic peptide analogue rotigaptide (formerly known as ZP123) [25].
• The vascular ANF-C receptor: role in atrial peptide signalling [26].
• As atrial natriuretic factor (ANF) is intimately involved in water and electrolyte homeostasis, dose-response studies were performed in the parotid as well as submaxillary glands of the rat with increasing doses of the atrial peptide to investigate its possible role as a sialogogic agent [27].

Analytical, diagnostic and therapeutic context of Atrial peptide

• Studies in man have confirmed that, when injected, they are natriuretic and that the plasma level, as measured by radioimmunoassay, changes with physiological changes in extracellular volume particularly those that occur with alteration of salt intake, the levels of atrial peptide rising as salt intake is increased [28].
• Atrial peptide natriuresis in the rat without genuine rise in filtration rate or wash-out of medullary electrolytes [29].
• The antiarrhythmic peptide rotigaptide (previously ZP123), which maintains gap junction intercellular communication, was tested in dogs subjected to a 60-min coronary artery occlusion and 4 h of reperfusion [30].
• The influence of the parasympathetic nervous system on the cardiovascular response to a synthetic atrial peptide (atriopeptin III) was examined in conscious normotensive rats by utilizing radiolabelled microspheres [23].
• The association between increasing N-terminal atrial peptide levels and operation age together with echocardiography findings support the clinical consensus of treating atrial septal defect patients in their childhood and adolescence [31].

References