Time course of release of atrial natriuretic peptide in the anaesthetized dog

1986 ◽  
Vol 64 (7) ◽  
pp. 1017-1022 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
A. J. Rankin ◽  
C. A. Courneya
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Time Course ◽  
Atrial Wall ◽  
Humoral Mechanism ◽  
Arterial Plasma ◽  
The Right ◽  
Atrial Receptors ◽  
Anaesthetized Dog ◽  
Atrial Natriuretic

In 12 chloralose anaesthetized dogs plasma concentration of immunoreactive atrial natriuretic peptide (IR-ANP) was measured using a radioimmunoassay. Plasma IR-ANP was 74 ± 4.8 pg/mL (mean ± SE) and increased by 39 ± 4.1 pg/mL when left atrial pressure was increased by 10 cm H2O during partial mitral obstruction. Observation of the time course of the changes in IR-ANP during atrial distension showed that IR-ANP was increased within 2 min of atrial distension and declined after atrial distension, with a half-time of 4.5 min. The time course of the changes in IR-ANP was unaffected by vagotomy or administration of atenolol. Maximum electrical stimulation of the right ansa subclavia failed to produce any change in IR-ANP. IR-ANP was higher in coronary sinus plasma than in femoral arterial plasma confirming that the heart was the source of the IR-ANP. The results support the hypothesis that IR-ANP is released from the heart by a direct effect of stretch of the atrial wall rather than by a neural or humoral mechanism involving a reflex from atrial receptors.

Adenosine modulates hypoxia-induced atrial natriuretic peptide release in fetal sheep

1995 ◽  
Vol 269 (1) ◽  
pp. H282-H287 ◽  
Author(s):  
D. A. Ogunyemi ◽  
B. J. Koos ◽  
C. P. Arora ◽  
L. C. Castro ◽  
B. A. Mason
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Fetal Hemoglobin ◽  
Blood Gases ◽  
Fetal Sheep ◽  
Control Value ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
The Right ◽  
Atrial Natriuretic

The effects of adenosine on atrial natriuretic peptide (ANP) secretion were determined in chronically catheterized fetal sheep (> 0.8 term). Adenosine was infused into the the right jugular vein for 1 h at 8 +/- 0.4 (5 fetuses), 160 +/- 8 (6 fetuses), and 344 +/- 18 micrograms.min-1.kg estimated fetal wt-1. Fetal arterial blood gases and pH were generally unaffected by adenosine, although mean arterial CO2 tension increased transiently by 2-5 Torr and pH fell progressively during the highest rate of infusion. During the intermediate and high infusion rates, fetal hemoglobin concentrations increased by 11-13% and mean fetal heart rate rose by 18% from a control value of approximately 167 beats/min. Mean arterial pressure was not affected during adenosine infusion. Adenosine significantly increased fetal plasma ANP levels, with maximum concentrations 1.80, 2.36, and 2.51 times greater than control means (142-166 pg/ml) for the respective infusion rates of 8, 160, and 344 micrograms.min-1.kg estimated fetal wt-1. In seven fetuses, reducing fetal arterial O2 tension by approximately 9-10 Torr from a control of 23 +/- 1.3 Torr increased plasma ANP concentrations approximately 2.4 times the control mean of 176 pg/min. Adenosine-receptor blockade with 8-(p-sulfophenyl)-theophylline reduced by 50% the maximum hypoxia-induced rise in plasma ANP concentrations. It is concluded that adenosine causes a dose-dependent rise in fetal plasma ANP concentrations and modulates fetal ANP release during hypoxia.

Intrarenal atrial natriuretic peptide infusion lowers arterial pressure chronically

1990 ◽  
Vol 259 (3) ◽  
pp. R585-R592 ◽  
Author(s):  
D. A. Hildebrandt ◽  
H. L. Mizelle ◽  
M. W. Brands ◽  
C. A. Gaillard ◽  
M. J. Smith ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Renal Artery ◽  
Natriuretic Peptide ◽  
Recovery Period ◽  
Arterial Plasma ◽  
Chronically Instrumented Dogs ◽  
Atrial Natriuretic

Chronic intravenous infusions of atrial natriuretic peptide (ANP) have been shown to lower mean arterial pressure (MAP) in both normal and hypertensive animals. However, the importance of the renal actions of ANP in mediating this hypotension is unknown. This study was designed to determine whether physiological or pathophysiological increases in intrarenal ANP levels influence long-term control of arterial pressure. ANP was infused into the renal artery of seven conscious, uninephrectomized, chronically instrumented dogs at 1, 2, and 4 ng.kg-1.min-1 for 7 days at each dose, followed by a recovery period. Then ANP was infused intravenously following the same protocol. MAP decreased from 88 +/- 3 to 78 +/- 3 mmHg during intrarenal infusion of 1 ng.kg-1.min-1 ANP; increasing the ANP infusion rate did not result in a further reduction in MAP. Systemic arterial plasma ANP concentration did not change from control (15 +/- 5 pg/ml) during 1 or 2 ng.kg-1.min-1 intrarenal ANP infusion but increased slightly during 4 ng.kg-1.min-1 intrarenal ANP infusion, averaging 53 +/- 11 pg/ml. Renal arterial plasma ANP concentrations were calculated to increase to approximately 120 +/- 5, 248 +/- 11, and 484 +/- 22 pg/ml during 1, 2, and 4 ng.kg-1.min-1 intrarenal ANP infusion, respectively. Intravenous ANP infusion did not alter MAP at 1 ng.kg-1.min-1, but MAP was slightly lower than control during 2 and 4 ng.kg-1.min-1 ANP infusion and remained below control during the postinfusion period.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Time course of released atrial natriuretic peptide after acute myocardial infarction.

1991 ◽  
Vol 55 (12) ◽  
pp. 1181-1186
Author(s):  
KAZUO NIITSUMA ◽  
MASAYOSHI SHIMIZU ◽  
TAKEO KAWAGUCHI ◽  
GENICHI NAKAGAMI ◽  
RYUICHI KIKAWADA
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Time Course ◽  
Atrial Natriuretic

Release of atrial natriuretic peptide by atrial distension

1985 ◽  
Vol 63 (6) ◽  
pp. 739-742 ◽  
Author(s):  
J. R. Ledsome ◽  
N. Wilson ◽  
C. A. Courneya ◽  
A. J. Rankin
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Pulmonary Vein ◽  
Natriuretic Peptide ◽  
Coronary Sinus ◽  
Femoral Artery ◽  
Left Atrial ◽  
Cervical Vagotomy ◽  
Atrial Receptors ◽  
Atrial Natriuretic

A heterologous radioimmunoassay was used to measure the concentration of immunoreactive atrial natriuretic peptide (iANP) in plasma from the femoral artery of eight chloralose anaesthetized dogs. Mitral obstruction which increased left atrial pressure by 11 cmH2O increased plasma iANP from 97 ± 10.3 (mean ± SE) to 135 ± 14.3 pg/mL. Pulmonary vein distension increased heart rate but did not increase plasma iANP. Bilateral cervical vagotomy and administration of atenolol (2 mg/kg) did not prevent the increase in iANP with mitral obstruction. Samples of blood from the coronary sinus had plasma iANP significantly higher than simultaneous samples from the femoral artery confirming the cardiac origin of the iANP. Release of iANP depends on direct stretch of the atrium rather than on a reflex involving left atrial receptors.

Bovine atrial natriuretic peptide in heart failure

1990 ◽  
Vol 124 (3) ◽  
pp. 463-467 ◽  
Author(s):  
N. Takemura ◽  
H. Koyama ◽  
T. Sako ◽  
K. Ando ◽  
S. Motoyoshi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Plasma Concentration ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Left Ventricular ◽  
Atrial Pressure ◽  
Right Atrial ◽  
The Right ◽  
Atrial Natriuretic

ABSTRACT The present study describes the concentration and molecular form of atrial natriuretic peptide (ANP) in Holstein dairy cattle with mild (bacterial endocarditis; BEC) or severe (dilated cardiomyopathy; DCM) heart failure. Significant increases in plasma concentration of ANP were observed in cattle with DCM (73·3 ± 16·02 pmol/l, n=4, P<0·01) and BEC (20·6± 3·45 pmol/l, n=7, P<0·05), when compared with those in control cattle (14·5± 1·84 pmol/l, n= 12). The concentration of ANP in cattle with DCM was significantly (P<0·01) higher compared with that in cattle with BEC. Plasma concentration of ANP correlated significantly with right atrial pressure (r =0·95, P<0·01) and left ventricular end-diastolic pressure (r= 0·84, P<0·01). Gel-permeation chromatography of ANP in plasma and the right atrium from control and cattle with BEC revealed a single peak corresponding to the elution position of authentic human ANP(99–126) in plasma, and two peaks corresponding to those of authentic human ANP(99–126) and pro-ANP in the atrial extract. In cattle with DCM, however, peaks corresponding to the elution positions of authentic human β-ANP and/or pro-ANP were detected in addition to the peak corresponding to ANP(99–126). The content of ANP in the right atrium of cattle with DCM was significantly (P<0·05) increased compared with that in control cattle and those with BEC. The present study therefore suggests that the synthesis and secretion of ANP might be stimulated by atrial distention induced by increased atrial pressure. This suggestion is supported by the fact that the middle molecular weight form of ANP, possibly corresponding to human β-ANP, was detected in both the plasma and atria of the cattle with severe heart failure. Journal of Endocrinology (1990) 124, 463–467

Vasorelaxation and vascular binding sites for atrial natriuretic peptide in pregnant rats

1988 ◽  
Vol 254 (6) ◽  
pp. H1027-H1033
Author(s):  
J. St-Louis ◽  
A. Parent ◽  
J. Gutkowska ◽  
J. Genest ◽  
E. L. Schiffrin
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Binding Sites ◽  
Female Rats ◽  
Pregnant Rats ◽  
Binding Characteristics ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed ◽  
The Right ◽  
Atrial Natriuretic

To investigate the role of atrial natriuretic peptide (ANP) in pregnancy, we measured, in cyclic and pregnant female rats (9- and 21-days pregnant), the vascular responsiveness to ANP using helical strips of the thoracic aorta, the binding characteristics of 125I-labeled ANP in a membrane preparation of the mesenteric vascular bed, and the plasma level and the atrial content of immunoreactive ANP (IR-ANP). On aorta strips, concentration-response (C-R) curves to phenylephrine (PE) were measured and were slightly displaced to the right in the aorta of both groups of pregnant rats in comparison with the cyclic rats. There was a potentiation of the relaxant response of ANP on the PE-precontracted aortic strips of 9-day pregnant rats but it was not statistically modified in tissues of 21-day pregnant rats in comparison with strips from cyclic rats. The number of binding sites (Bmax) for ANP in the mesenteric vascular bed was similar in cyclic rats and the two groups of pregnant rats. The dissociation constant (KD) of ANP was lower in 9-day pregnant rats than in cyclic and 21-day pregnant ones. Plasma IR-ANP was not different in 9-day pregnant rats and cyclic rats but was markedly decreased at the end of gestation. Atrial content of IR-ANP increased at the end of gestation, but not in midpregnancy in comparison with cyclic rats. These results indicate that despite the reported important increase in blood volume during gestation the secretion of ANP is not increased and suggest that the ANP-volume relationship is reset during pregnancy in the rat.

Atrial natriuretic peptide release from the ventricles in response to exercise in dogs with atrioventricular block

1994 ◽  
Vol 72 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Louise Béliveau ◽  
François Péronnet ◽  
Daniel G. Bichet ◽  
Réginald Nadeau
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrioventricular Block ◽  
Right Atrial ◽  
Ventricular Rate ◽  
Complete Atrioventricular Block ◽  
Arterial Plasma ◽  
Complete Atrioventricular ◽  
Rest And Exercise ◽  
Atrial Natriuretic

The purpose of this study was to examine atrial natriuretic peptide (ANP) secretion at rest and in response to moderate treadmill exercise (10 min, 4 km/h, 26% slope) in control dogs (n = 17) and in dogs (n = 14) with complete atrioventricular block produced by electrocauterization of the His bundle. Atrial rates were similar in both groups (103 ± 13 vs. 102 ± 9 beats/min at rest and 162 ± 10 vs. 160 ± 17 beats/min at exercise in control dogs and in dogs with atrioventricular block, respectively; mean ± SE), but ventricular rate was markedly lower in dogs with atrioventricular block (47 ± 9 and 61 ± 10 beats/min at rest and exercise, respectively). The lower ventricular rate was associated with an increased cardiac preload, as evidenced by the higher right atrial pressure in dogs with atrioventricular block at rest (2.2 ± 1.4 vs. 1.1 ± 0.9 mmHg; p < 0.05) and exercise (7.6 ± 3.1 vs. 4.2 ± 1.7 mmHg; p < 0.05). Arterial plasma ANP concentrations were markedly higher at rest (151 ± 21 vs. 36 ± 10 pg/mL; p < 0.05) and exercise (353 ± 31 vs. 72 ± 17 pg/mL; p < 0.05) in dogs with atrioventricular block. This observation supports the hypothesis that atrial wall stretching is a major stimulus for ANP release at rest and exercise. Ventricular release of ANP could also contribute to the higher plasma ANP concentrations observed both at rest and during exercise in dogs with complete atrioventricular block. Indeed, a large ANP concentration gradient was measured between the aorta and the distal part of the coronary sinus in these dogs at rest (227 ± 55 pg/mL) and exercise (240 ± 57 pg/mL) but not in control dogs. Changes in heart rate and in vasopressin and catecholamine concentrations do not appear to play a major role in the control of ANP release. Finally, the higher arterial ANP concentrations in dogs with complete atrioventricular block do not modify the activity of the renin–angiotensin–aldosterone system at rest, nor its response to exercise.Key words: catecholamines, aldosterone, vasopressin, natriuretic peptide.

Atrial natriuretic peptide in brain and pituitary gland

1997 ◽  
Vol 77 (2) ◽  
pp. 465-515 ◽  
Author(s):  
J. Gutkowska ◽  
J. Antunes-Rodrigues ◽  
S. M. McCann
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Brain Stem ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Volume Expansion ◽  
Body Fluid ◽  
Fluid Homeostasis ◽  
Body Fluid Homeostasis ◽  
The Right ◽  
Atrial Natriuretic

The data reviewed establish the presence and important role in body fluid homeostasis of brain atrial natriuretic peptide (ANP) in all vertebrate-species examined. The peptide is localized in neurons in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation, and its receptors are located in regions that contain the peptide. Most, if not all, of the actions of ANP are mediated by activation of particulate guanylyl cyclase with generation of guanosine 3',5'-cyclic monophosphate, which mediates its actions in brain as in the periphery. Although atrial stretch releases ANP from cardiac myocytes, the experiments indicate that the response to acute blood volume expansion is markedly reduced after elimination of neural control. Volume expansion distends baroreceptors in the right atria, carotid-aortic sinuses, and kidney, altering afferent input to the brain stem and hence the hypothalamus, resulting in stimulation via ANPergic neurons in the hypothalamus of oxytocin release from the neurohypophysis that circulates to the right atrium to stimulate ANP release. The ANP circulates to the kidney and induces natriuresis. Atrial natriuretic peptide also induces vasodilation compensating rapidly for increased blood volume by increased vascular capacity. Atrial natriuretic peptide released into hypophysial portal blood vessels inhibits release of adrenocorticotropic hormone (ACTH), thereby decreasing aldosterone release and enhancing natriuresis. Furthermore, the ANP neurons inhibit AVP release leading to diuresis and decreased ACTH release. Activation of hypothalamic ANPergic neurons via volume expansion also inhibits water and salt intake. These inhibitory actions may be partially mediated via ANP neurons in the olfactory system altering salt taste. Atrial natriuretic peptide neurons probably also alter fluid movement in the choroid plexus and in other brain vascular beds. Therefore, brain ANP neurons play an important role in modulating not only intake of body fluids, but their excretion to maintain body fluid homeostasis.

Effects of autonomic stimulation on plasma immunoreactive atrial natriuretic peptide in the anesthetized rabbit

1987 ◽  
Vol 65 (4) ◽  
pp. 532-537 ◽  
Author(s):  
A. J. Rankin ◽  
N. Wilson ◽  
J. R. Ledsome
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Vagus Nerve ◽  
Cardiac Myocytes ◽  
Natriuretic Peptide ◽  
Direct Action ◽  
Cervical Ganglion ◽  
Significant Change ◽  
The Right ◽  
Stimulation Of ◽  
Atrial Natriuretic

Infusions of norepinephrine led to a significant sevenfold increase in plasma immunoreactive atrial natriuretic peptide, while infusions of acetylcholine caused no significant change in the level of the peptide. Efferent stimulation of the right vagus nerve or right inferior cervical ganglion in anesthetized, vagotomized rabbits produced no significant changes in the immunoreactive atrial natriuretic peptide. The findings suggest that the mechanism by which norepinephrine releases immunoreactive atrial natriuretic peptide is not the result of a direct action on the cardiac myocytes.

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