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.

Haemodynamic and Hormonal Responses to Cardiac Pacing in Humans: Influence of Different Stimulation Sequences and Rates

1995 ◽  
Vol 88 (2) ◽  
pp. 165-172 ◽  
Author(s):  
Hans Berglund ◽  
Anders Edlund ◽  
Elvar Theodorsson ◽  
Hans Vallin
Keyword(s):  
Plasma Concentration ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Pulmonary Capillary ◽  
Peptide Release ◽  
Arterial Plasma ◽  
Wedge Pressure ◽  
Atrial Natriuretic

1. To examine the effects of rate and pressure on release of vasoactive hormones, 10 healthy subjects were examined. 2. A standardized pacing protocol was used to achieve different haemodynamic responses at two predetermined heart rates. Haemodynamic variables, and plasma concentrations of atrial natriuretic peptide, arginine vasopressin, adrenaline and noradrenaline were measured. 3. Right atrioventricular pacing at a rate of 150 impulses/min resulted in disparate responses in right atrial pressure (slight decrease) and pulmonary capillary wedge pressure (increase). Change in arterial plasma concentration of atrial natriuretic peptide correlated to change in pulmonary capillary wedge pressure, and change in arterial plasma concentration of noradrenaline correlated to change in total systemic vascular resistance, whereas concentrations of adrenaline and arginine vasopressin did not alter significantly during the stimulation periods. A significant influence of rate in addition to the pressure related influence on plasma concentration of atrial natriuretic peptide was found. In contrast, an increase in rate in the absence of an increase in atrial pressures did not raise the plasma concentration of atrial natriuretic peptide. There was no significant relationship between change in atrial natriuretic peptide and noradrenaline. 4. These data support the concept of a rate dependence of atrial natriuretic peptide release in man. Increased atrial pressure and thus presumed atrial stretch seems to be a prerequisite for increased plasma concentration of atrial natriuretic peptide. In addition, these results highlight the importance of monitoring both left and right atrial pressure in clinical investigations assessing modulation of atrial natriuretic peptide release.

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.

A premature low-birth-weight infant with congenital complete atrioventricular block and myocarditis successfully treated by staged pacemaker implantation

2016 ◽  
Vol 26 (5) ◽  
pp. 1029-1032
Author(s):  
Tao Fujioka ◽  
Masaki Nii ◽  
Yasuhiko Tanaka
Keyword(s):  
Birth Weight ◽  
Low Birth Weight ◽  
Atrioventricular Block ◽  
Pacemaker Implantation ◽  
Myocardial Damage ◽  
Ventricular Rate ◽  
Complete Atrioventricular Block ◽  
Low Birth Weight Infant ◽  
Congenital Complete Atrioventricular Block ◽  
Complete Atrioventricular

AbstractCongenital complete atrioventricular block is a known lethal condition. Although antenatal diagnosis and the technical advances of pacemaker treatment have reduced its mortality, treatment of premature babies with significant myocardial damage remains a challenge. In this paper, we report the case of a premature low-birth-weight infant with congenital complete atrioventricular block and extremely low ventricular rate, fetal hydrops, and myocarditis who was successfully treated with staged permanent pacemaker implantation.

Hemodynamic and renal effects of low-dose infusions of atrial peptide in awake dogs

1988 ◽  
Vol 254 (2) ◽  
pp. R161-R169 ◽  
Author(s):  
P. Bie ◽  
B. C. Wang ◽  
R. J. Leadley ◽  
K. L. Goetz
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urine Flow ◽  
Right Atrial ◽  
Experimental Protocols ◽  
Cardiac Filling ◽  
Left And Right ◽  
Atrial Natriuretic

The effects of alpha-human atrial natriuretic peptide (alpha-hANP) on cardiovascular and renal function in conscious dogs were evaluated in two experimental protocols. In one protocol, alpha-hANP was infused intravenously at increasing rates of 50, 100, and 200 ng.min-1.kg-1 (stepup infusion) during successive 20-min periods. The greatest responses occurred during the final 20-min period of the stepup infusion when the plasma concentration of immunoreactive atrial natriuretic peptide (irANP) was increased by 44-fold over preinfusion values; pressures in the aorta and both atria were decreased at this time, whereas glomerular filtration rate, urine flow, and sodium excretion were increased. In a second protocol, alpha-hANP was infused for 1 h at constant rates of either 12.5, 25, or 50 ng.min-1.kg-1; these constant infusions increased plasma irANP by 3-, 7-, and 12-fold, respectively. Each infusion rate decreased left and right atrial pressures and increased urine flow and sodium excretion. The two lowest infusion rates elevated plasma irANP to levels that would be expected to occur only during unusual physiological, or perhaps pathophysiological, conditions. The two highest infusion rates decreased plasma renin activity. Nevertheless, the accompanying maximal increases in sodium excretion were modest (41-72%). These data imply that small changes in circulating atrial peptides that presumably occur under normal physiological conditions would not have a dominant effect on the regulation of sodium excretion; the peptides may, however, play a modulatory role on sodium excretion under these conditions. It remains to be determined whether the ability of atrial peptides to lower cardiac filling pressures is of physiological significance.

Mechanism for decrease in cardiac output with atrial natriuretic peptide in dogs

1989 ◽  
Vol 256 (3) ◽  
pp. H760-H765 ◽  
Author(s):  
R. W. Lee ◽  
S. Goldman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Right Atrial ◽  
Total Blood Volume ◽  
Total Blood ◽  
Atrial Natriuretic

To examine the mechanism by which atrial natriuretic peptide (ANP) decreases cardiac output, we studied changes in the heart, peripheral circulation, and blood flow distribution in eight dogs. ANP was given as a bolus (3.0 micrograms/kg) followed by an infusion of 0.3 microgram.kg-1.min-1. ANP did not change heart rate, total peripheral vascular resistance, and the first derivative of left ventricular pressure but decreased mean aortic pressure from 91 +/- 4 to 76 +/- 3 mmHg (P less than 0.001) and cardiac output from 153 +/- 15 to 130 +/- 9 ml.kg-1.min-1 (P less than 0.02). Right atrial pressure and left ventricular end-diastolic pressure also decreased. Mean circulatory filling pressure decreased from 7.1 +/- 0.3 to 6.0 +/- 0.3 mmHg (P less than 0.001), but venous compliance and unstressed vascular volume did not change. Resistance to venous return increased from 0.056 +/- 0.008 to 0.063 +/- 0.010 mmHg.ml-1.kg.min (P less than 0.05). Arterial compliance increased from 0.060 +/- 0.003 to 0.072 +/- 0.004 ml.mmHg-1.kg-1 (P less than 0.02). Total blood volume and central blood volume decreased from 82.2 +/- 3.1 to 76.2 +/- 4.6 and from 19.8 +/- 0.8 to 17.6 +/- 0.6 ml/kg (P less than 0.02), respectively. Blood flow increased to the kidneys. We conclude that ANP decreases cardiac output by decreasing total blood volume. This results in a lower operating pressure and volume in the venous capacitance system with no significant venodilating effects. Cardiac factors and a redistribution of flow to the splanchnic organs are not important mechanisms to explain the decrease in cardiac output with ANP.

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)

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