scholarly journals Multiple plasma proteins control atrial natriuretic peptide (ANP) aggregation

2004 ◽  
Vol 33 (2) ◽  
pp. 335-341 ◽  
Author(s):  
C Torricelli ◽  
E Capurro ◽  
A Santucci ◽  
A Paffetti ◽  
C D’Ambrosio ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mass Spectrometry Analysis ◽  
High Density Lipoproteins ◽  
Protective Mechanism ◽  
Two Dimensional Gel Electrophoresis ◽  
Spectrometry Analysis ◽  
Dimeric Form ◽  
Atrial Natriuretic

We have recently demonstrated that human α-atrial natriuretic peptide (α-hANP), an amyloidogenic peptide responsible for isolated atrial amyloidosis, binds to a dimeric form of apo A-I belonging to small high-density lipoproteins (HDL). This binding phenomenon is considered a protective mechanism since it inhibits or strongly reduces the ANP aggregation process. The observation that plasma exhibits at least four times greater amyloid inhibitory activity than HDL prompted us to determine whether small HDL are the only ANP plasma-binding factors. After incubation of whole plasma with labelled ANP, the macromolecular complexes were subjected to two-dimensional gel electrophoresis followed by autoradiography. The results presented here provide novel evidence of additional binding proteins, in addition to apo A-I dimer, able to bind ANP in vitro and to prevent its aggregation. The mass spectrometry analysis of the radioactive spots identified them as albumin, α-1 antitrypsin, orosomucoid and apo A-IV-TTR complex. The putative impact of these findings in the amyloidogenic/antiamyloidogenic peptides network is discussed.

scholarly journals Differential effects of doxorubicin on atrial natriuretic peptide expression in vivo and in vitro

2001 ◽  
Vol 34 (3-4) ◽  
Author(s):  
ASIM RAHMAN ◽  
MAHMOOD ALAM ◽  
SUDHA RAO ◽  
LIN CAI ◽  
CLARK LUTHER T. ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Differential Effects ◽  
Peptide Expression ◽  
Atrial Natriuretic

Isoproterenol induces release of atrial natriuretic peptide from rat atrium in vitro

1992 ◽  
Vol 262 (1) ◽  
pp. H285-H292 ◽  
Author(s):  
G. Agnoletti ◽  
A. Rodella ◽  
A. Cornacchiari ◽  
A. F. Panzali ◽  
P. Harris ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mechanical Stimulation ◽  
The Other ◽  
Mechanical Activity ◽  
Mechanical Function ◽  
Rat Atria ◽  
Rat Atrium ◽  
Atrial Natriuretic

To investigate the mechanism underlying the release of atrial natriuretic peptide (ANP) in in vitro condition, isolated, superfused rat atria were subjected to adrenergic, chronotropic, and mechanical stimulation. First administration of isoproterenol (Iso; either 10(-9) or 10(-6) M) caused a release of ANP, which was transient. Subsequent increments in concentration of Iso always resulted in a much lower release of ANP, despite the increased effects on the mechanical function of the atria. Stretching of the atria resulted in a transient release of ANP. Subsequent increments in stretching were followed by decreasing release of ANP. The total score of ANP in atrial tissue after Iso and stretching was not measurably depleted. Pacing the atria with increasing frequency did not induce release of ANP. Depolarization with 40 mM KCl abolished the release of ANP in response to Iso but not the release induced by stretch. In the presence of low external Ca2+, which abolished mechanical activity, both Iso and stretch could still induce release of ANP. Propranolol abolished the release of ANP by Iso but not that induced by stretching. Prazosin did not affect the release by either stretch or Iso. Stretching the atria 20 min after administration of Iso did not cause any further release of ANP. On the other hand, adding Iso 20 min after stretching induced a release of ANP. It is concluded that Iso and stretch cause a transient release from isolated strips of atria. The amount of ANP released is not related to the dose of Iso or to the load applied. Mechanisms involved in the release mediated by the two stimuli are different.(ABSTRACT TRUNCATED AT 250 WORDS)

Direct effect of α-human atrial natriuretic peptide on human vasculature in vivo and in vitro

1988 ◽  
Vol 74 (2) ◽  
pp. 207-211 ◽  
Author(s):  
A. Hughes ◽  
S. Thom ◽  
P. Goldberg ◽  
G. Martin ◽  
P. Sever
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Forearm Blood Flow ◽  
Renin Angiotensin System ◽  
Organ Bath ◽  
Human Atrial Natriuretic Peptide ◽  
Atrial Natriuretic

1. The effect of a α-human atrial natriuretic peptide (1–28) (ANP) on human vasculature was investigated in vivo and in vitro. Possible involvement of vascular dopamine receptors and the renin-angiotensin system in the response to ANP was also studied in vivo. 2. Forearm blood blow was measured by venous occlusion plethysmography. Isolated human blood vessels were studied using conventional organ bath techniques. 3. ANP (0.1–1 μg/min, intra-arterially) produced a dose-dependent increase in forearm blood flow, corresponding to a 163% increase in net forearm blood flow in the study arm. This action of ANP was not antagonized by (R)-sulpiride (100 μg/min, intra-arterially), a selective vascular dopamine receptor antagonist, or 50 mg of oral captopril, an inhibitor of angiotensin-converting enzyme. 4. ANP (1 nmol/l–1 μmol/l) produced concentration-dependent relaxation of isolated human arteries, including brachial artery, but was without effect on isolated human saphenous vein. 5. ANP produces vasodilatation in vivo and relaxes isolated human arterial smooth muscle. This action of ANP may contribute to its reported hypotensive effects in vivo.

Renal hemodynamic and natriuretic effects of manganese and interactions with atrial natriuretic peptide

1990 ◽  
Vol 258 (4) ◽  
pp. F998-F1004 ◽  
Author(s):  
H. M. Lafferty ◽  
M. Gunning ◽  
H. R. Brady ◽  
B. M. Brenner ◽  
S. Anderson
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Plasma Flow ◽  
Collecting Duct ◽  
Hydraulic Pressure ◽  
Cgmp Production ◽  
Atrial Natriuretic

Manganese (Mn2+) is a cofactor for guanylate cyclase (GC), which is involved in the generation of guanosine 3',5'-cyclic monophosphate (cGMP), a second messenger for atrial natriuretic peptide (ANP) action. Mn2+ is also, however, a nonselective calcium-channel blocker. We examined the effects of infusion of MnCl2 into normal rats and its interaction in vivo and in vitro with GC and ANP. MnCl2 significantly increased glomerular filtration rate (GFR) and effective renal plasma flow rate (RPF). These effects were caused by selective afferent arteriolar vasodilatation, which allowed the glomerular capillary plasma flow rate and hydraulic pressure to rise, thus elevating single-nephron GFR. Urinary Na+ excretion (UNaV) also increased with MnCl2. The natriuresis was, unlike ANP, not mediated by GC activation and cGMP production, as MnCl2 had no effect on either urinary cGMP excretion or cGMP accumulation in intact inner medullary collecting duct cell (IMCD) suspensions, nor did it affect Na(+)-dependent oxygen consumption in these cells. When superimposed on an infusion of ANP, MnCl2 resulted in significant increases in UNaV, GFR, and RPF. These effects were associated with small but significant increments in urinary cGMP excretion. However, MnCl2 did not affect in vitro cGMP production in intact IMCDs or glomeruli in response to ANP stimulation. It is uncertain therefore whether the in vivo augmentation of the natriuretic effect of ANP by MnCl2 is related to GC activation and cGMP production.

scholarly journals Atrial Natriuretic Peptide Improves Neurite Outgrowth from Spiral Ganglion Neurons In Vitro through a cGMP-Dependent Manner

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Fei Sun ◽  
Ke Zhou ◽  
Ke-yong Tian ◽  
Jie Wang ◽  
Jian-hua Qiu ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Neurite Outgrowth ◽  
Natriuretic Peptide ◽  
Critical Role ◽  
Spiral Ganglion ◽  
Spiral Ganglion Neurons ◽  
Dependent Manner ◽  
Ganglion Neurons ◽  
Atrial Natriuretic

The spiral ganglion neurons (SGNs) are the primary afferent neurons in the spiral ganglion (SG), while their degeneration or loss would cause sensorineural hearing loss. As a cardiac-derived hormone, atrial natriuretic peptide (ANP) plays a critical role in cardiovascular homeostasis through binding to its functional receptors (NPR-A and NPR-C). ANP and its receptors are widely expressed in the mammalian nervous system where they could be implicated in the regulation of multiple neural functions. Although previous studies have provided direct evidence for the presence of ANP and its functional receptors in the inner ear, their presence within the cochlear SG and their regulatory roles during auditory neurotransmission and development remain largely unknown. Based on our previous findings, we investigated the expression patterns of ANP and its receptors in the cochlear SG and dissociated SGNs and determined the influence of ANP on neurite outgrowth in vitro by using organotypic SG explants and dissociated SGN cultures from postnatal rats. We have demonstrated that ANP and its receptors are expressed in neurons within the cochlear SG of postnatal rat, while ANP may promote neurite outgrowth of SGNs via the NPR-A/cGMP/PKG pathway in a dose-dependent manner. These results indicate that ANP would play a role in normal neuritogenesis of SGN during cochlear development and represents a potential therapeutic candidate to enhance regeneration and regrowth of SGN neurites.

Effect of atrial natriuretic peptide on catecholamine release from human pheochromocytoma

1989 ◽  
Vol 120 (1) ◽  
pp. 107-112 ◽  
Author(s):  
Mitsuaki Nakamaru ◽  
Toshio Ogihara ◽  
Hiroshi Saito ◽  
Hiromi Rakugi ◽  
Kiyoko Hashizume ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Plasma Catecholamines ◽  
Normal Subjects ◽  
Catecholamine Release ◽  
Plasma Norepinephrine ◽  
Atrial Natriuretic

Abstract. The effect of synthetic alpha human atrial natriuretic peptide on catecholamine release from human pheochromocytomas was studied both in vivo and in vitro. Iv infusion of atrial natriuretic peptide at a rate of 0.1 μg ·kg−1·min−1 for 60 min into two normotensive patients with pheochromocytoma caused a small decrease in the mean blood pressure, increase in the heart rate, and marked increase in the plasma level of norepinephrine (2.08 to 6.83 nmol/l, and 1.15 to 2.83 nmol/l, respectively) compared with 0.60 ± 0.10 to 1.19 ± 0.20 nmol/l in normal subjects. Treatment with atrial natriuretic peptide also increased the plasma epinephrine level from 0.34 to 1.27 nmol/l, and from 0.67 to 0.79 nmol/l in the patients with pheochromocytoma, but not in the normal subjects (0.05 ± 0.01 to 0.05 ± 0.01 nmol/l). After removal of the tumour, the responses of the plasma norepinephrine and epinephrine to atrial natriuretic peptide infusion were normalized. There was no significant effect of 10−8 to 10−5 mol/l atrial natriuretic peptide on the basal release of catecholamines from isolated superfused pheochromocytoma tissue. Atrial natriuretic peptide (10−7 mol/l) did not affect the increase in catecholamine release induced by glucagon (10−5 mol/l). These results suggest that the exaggerated responses of plasma catecholamines to atrial natriuretic peptide in patients with pheochromocytoma may be due to a washout effect resulting from change in blood flow in the vessels feeding the tumour rather than increased sympathetic nerve activity induced by hypotension and hypovolemia. The results also suggest that atrial natriuretic peptide dose not have any direct action on pheochromocytoma tissue causing catecholamine release.

Ischemia stimulates the release of atrial natriuretic peptide from rat cardiac ventricular myocardium in vitro

Life Sciences ◽  
1992 ◽  
Vol 50 (5) ◽  
pp. 365-373 ◽  
Author(s):  
Paavo A. Uusimaa ◽  
Keijo J. Peuhkurinen ◽  
Ilmo E. Hassinen ◽  
Olli Vuolteenaho ◽  
Heikki Ruskoaho
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Ventricular Myocardium ◽  
Atrial Natriuretic
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