The effect of short-lasting atrial pacing on the release of atrial natriuretic peptide, vasopressin, and methionine enkephalin in man

1987 ◽  
Vol 116 (2) ◽  
pp. 235-240 ◽  
Author(s):  
Kozo Ota ◽  
Tokihisa Kimura ◽  
Meiichi Ito ◽  
Minoru Inoue ◽  
Masaru Shoji ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Atrial Pacing ◽  
Methionine Enkephalin ◽  
Arterial Blood ◽  
The Right ◽  
Atrial Natriuretic

Abstract. In order to study the effect of atrial tachycardia on the release of atrial natriuretic peptide (ANP), AVP, and methionine enkephalin (M-Enk), plasma concentrations of these peptides in the right ventricle were determined in patients with various arrhythmias (N = 10) during cardiac catheterization and incremental atrial pacing. Each pacing (100 per min, the maximum rate for 1:1 atrioventricular conduction, and 200 per min) lasted 4 to 5 min. Plasma ANP was significantly increased from 53.1 ± 12.2 in the resting condition to 168.9 ± 59.9 pmol/l at a pacing rate of 200 beats per min (P < 0.05); plasma AVP tended to decrease, but not significantly, and plasma M-Enk did not change at all. Pulse pressure in the right atrium (PPRA) and mean right atrial pressure (MRAP) tended to increase during the pacing, and at the rate of 200 beats per min PPRA was significantly higher than at the rate of 100 beats per min. Mean arterial blood pressure, plasma osmolality, and plasma sodium and potassium concentrations did not change significantly. There were significant correlations between plasma ANP and PPRA, MRAP and heart rate. These results indicate that atrial pacing stimulates ANP release with a rise in right atrial pressure, but does not influence M-Enk and AVP releases.

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

EFFECTS OF INCREMENTAL PEEP ON ATRIAL NATRIURETIC PEPTIDE, RIGHT ATRIAL PRESSURE AND ECHOCARDIOGRAPHIC DIMENSIONS IN MAN

1989 ◽  
Vol 71 (Supplement) ◽  
pp. A1129
Author(s):  
J. Scholz ◽  
F. Bednarz ◽  
N. Roewer ◽  
R. Schmidt ◽  
J. Schulte am Esch
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Atrial Natriuretic

Role of atrial pressure and rate in release of atrial natriuretic peptide

1988 ◽  
Vol 254 (4) ◽  
pp. R607-R610 ◽  
Author(s):  
K. P. Walsh ◽  
T. D. Williams ◽  
C. Spiteri ◽  
E. Pitts ◽  
S. L. Lightman ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Coronary Sinus ◽  
Vena Cava ◽  
Balloon Occlusion ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Atrial Rate ◽  
Atrial Natriuretic

To investigate whether atrial natriuretic peptide (ANP) release during paroxysmal tachycardia is due to increased atrial rate or increased atrial pressure, plasma ANP concentrations were measured during atrial pacing at increasing rates in six alpha-chloralose-anesthetized dogs whose atrial pressures were maintained artificially low by balloon occlusion of the inferior vena cava (IVC). These ANP concentrations were compared with those seen during identical increasing atrial rates in the same dogs without IVC occlusion. During incremental pacing without IVC occlusion, pulmonary wedge pressure (PWP; mean +/- SE) rose progressively from 5.3 +/- 1.6 at 200 to 20.2 +/- 2.3 mmHg at 350 beats/min (P less than 0.01), and right atrial pressure (RAP) rose progressively from 2.5 +/- 0.9 at 200 to 6.7 +/- 2.1 mmHg at 350 beats/min (P less than 0.05). At the same time, arterial and coronary sinus ANP concentrations rose from 116 +/- 55 and 339 +/- 91 to 1,126 +/- 226 and 1,960 +/- 456 pmol/l, respectively (P less than 0.01). In contrast, incremental pacing with IVC occlusion produced no significant increase in PWP and RAP. Arterial and coronary sinus ANP concentrations during IVC occlusion were, respectively, 208 +/- 126 and 388 +/- 159 at 200 and 261 +/- 83 and 345 +/- 80 pmol/l at 350 beats/min (NS). This study demonstrates that the release of ANP during tachycardia is primarily dependent on increased atrial pressure and not atrial rate.

Hemorrhage effects on plasma ANP, NH2-terminal pro-ANP, and pressor hormones in anesthetized and conscious rats

1994 ◽  
Vol 266 (6) ◽  
pp. R1933-R1943 ◽  
Author(s):  
H. Leskinen ◽  
H. Ruskoaho ◽  
P. Huttunen ◽  
J. Leppaluoto ◽  
O. Vuolteenaho
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Right Atrial Pressure ◽  
Conscious Rats ◽  
Anesthetized Rats ◽  
Atrial Natriuretic

We examined the effect of hemorrhage on plasma NH2-terminal pro-atrial natriuretic peptide (NT-pro-ANP) and atrial natriuretic peptide (ANP) in anesthetized and conscious rats. Blood (1.5 ml/time point) was withdrawn at 0, 10, 20, and 30 min. In anesthetized rats it caused decrease in mean arterial pressure and led to bradycardia in 2 min. Right atrial pressure decreased significantly after 12 min. However, plasma ANP did not change, and NT-pro-ANP actually increased from 481 +/- 55 to 609 +/- 73 pmol/l (P < 0.01) at 20 min and to 696 +/- 82 pmol/l (P < 0.01) at 30 min. Also plasma arginine-8-vasopressin (AVP) and epinephrine increased significantly at 30 min. No significant changes in plasma endothelin and norepinephrine were found. The increase in NT-pro-ANP after hemorrhage was not blocked by AVP V1-receptor, alpha- and beta-catecholaminergic receptor, or muscarinic-receptor antagonists. The plasma 125I-ANP disappearance curve was shifted to the right after hemorrhage in anesthetized rats, suggesting that the elimination of ANP was decreased. In conscious rats, heart rate and right atrial pressure did not change significantly after hemorrhage, and mean arterial pressure did not decrease until 22 min. NT-pro-ANP decreased from 1,467 +/- 146 to 1,072 +/- 130 pmol/l (P < 0.01) at 20 min and to 941 +/- 41 pmol/l (P < 0.01) at 30 min. Plasma ANP did not respond to hemorrhage in conscious rats. In conclusion, we found no change in plasma ANP during hemorrhage in either anesthetized or conscious rats, but we did find a significant increase in plasma NT-pro-ANP levels in anesthetized rats and a significant decrease in conscious rats. We suggest that this divergence may be due to different hemodynamic responses to hemorrhage.

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.

Atrial natriuretic peptide response to rapid atrial pacing in cardiac-denervated dogs

1989 ◽  
Vol 257 (1) ◽  
pp. R162-R167 ◽  
Author(s):  
T. D. Williams ◽  
K. P. Walsh ◽  
R. Canepa-Anson ◽  
M. I. Noble ◽  
A. J. Drake-Holland ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Flow Rate ◽  
Free Water ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Cardiac Denervation ◽  
Atrial Natriuretic

The effects of rapid atrial pacing on central hemodynamics, plasma hormones, and renal function were investigated in eight control and nine cardiac-denervated dogs under chloralose anesthesia. Pacing at approximately 250 ppm for 60 min caused similar increases in pulmonary wedge and right atrial pressures, systemic vascular resistance, and plasma atrial natriuretic peptide (ANP) in both groups. In control dogs, pacing produced a fall in both plasma vasopressin (AVP) and plasma renin activity (PRA) and a rise in urine flow rate associated with an increase in free water but not sodium clearance. In contrast, in cardiac-denervated dogs, both plasma AVP and PRA increased during pacing; urine flow rate did not change, and marked sodium retention occurred. This study supports the concept that the increase in urine flow during rapid atrial pacing is mediated by inhibition of renin and AVP secretion through intact cardiac nerves. The secretion of ANP is unaffected by cardiac denervation. The natriuretic and vasodilator actions of high plasma ANP concentrations during rapid atrial pacing can be inhibited either by neurally mediated cardiorenal effects in normal animals or by stimulation of the renin-angiotensin system after cardiac denervation.

Sign in / Sign up

Export Citation Format

Share Document