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

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.

1990 ◽  
Vol 124 (3) ◽  
pp. 463-467 ◽  
Author(s):  
N. Takemura ◽  
H. Koyama ◽  
T. Sako ◽  
K. Ando ◽  
S. Motoyoshi ◽  
...  

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


Cardiology ◽  
1991 ◽  
Vol 78 (4) ◽  
pp. 304-310 ◽  
Author(s):  
A. Michelucci ◽  
L. Padeletti ◽  
A. Monopoly ◽  
G. Fabbri ◽  
C. Tostiguerra ◽  
...  

1987 ◽  
Vol 73 (5) ◽  
pp. 459-462 ◽  
Author(s):  
P. Erne ◽  
A. E. G. Raine ◽  
E. Burgisser ◽  
E. Gradel ◽  
F. Burkart ◽  
...  

1. To determine the influence of loss of atrioventricular synchrony on release of atrial natriuretic peptide (ANP), plasma ANP concentrations were measured by radioreceptor assay in 16 patients during sequential and ventricular cardiac pacing at normal heart rates. 2. Ventricular pacing induced an increase in plasma ANP concentrations (means ± SEM) from 44 ± 3 to 104 ± 4 pmol/l (P < 0.01) in 11 patients in whom systemic blood pressure was maintained. 3. In contrast, when ventricular pacing was associated with a fall in blood pressure (five patients), ANP levels (means ± SEM) fell from 68 ± 6 to 14 ± 4 pmol/l (n = 5, P < 0.05) within 5 min, despite an increase in atrial pressure. Plasma catecholamines also rose significantly in these latter patients. 4. We conclude that when loss of atrioventricular synchrony is well tolerated haemodynamically, cardiac release of ANP is increased in keeping with elevation in atrial pressure. However, the fall in plasma ANP concentration observed when ventricular pacing produces a fall in blood pressure suggests that in addition to atrial pressure, ANP release may be influenced by negative feedback mechanisms, possibly involving the baroreflex and autonomic nervous system.


1998 ◽  
Vol 95 (2) ◽  
pp. 195-202 ◽  
Author(s):  
Daniel D. BORGESON ◽  
Tracy L. STEVENS ◽  
Denise M. HEUBLEIN ◽  
Yuzuru MATSUDA ◽  
John C. BURNETT

1.A family of structurally related but genetically distinct natriuretic peptides exist which include atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) of myocardial cell origin and C-type natriuretic peptide (CNP) of endothelial and renal epithelial cell origin. All three exert actions via cGMP, with ANP and BNP functioning via the natriuretic peptide A receptor and CNP via the natriuretic peptide B receptor. 2.Circulating and urinary natriuretic peptides were determined in response to acute intravascular volume overload (AVO). Additionally, their functional role in cardiorenal regulation during AVO was investigated by utilizing the natriuretic peptide receptor antagonist HS-142-1. Control (n = 5) and study dogs (HS-142-1, n = 9) underwent AVO with normal saline equal to 10% of body weight over 1 ;h. Both groups demonstrated similar significant increases in right atrial pressure, pulmonary capillary wedge pressure, pulmonary artery pressure and cardiac output. Circulating ANP paralleled increases in right atrial pressure and pulmonary capillary wedge pressure, with no changes in plasma BNP or CNP. At peak AVO, urinary CNP excretion was increased compared with baseline (7.0±4.2 versus 62±8.0 ;pg/min, P< 0.05). 3.In the HS-142-1-treated group, plasma cGMP was decreased compared with the control group (9.6±1.1 to 5.0±1.2 ;pmol/ml, P< 0.05). A significant attenuation of natriuresis (566±91 versus 1241±198 ;μEq/min, P< 0.05) and diuresis (4.8±0.7 versus 10.1±2.0 ;ml/min, P< 0.05) was also observed at peak AVO in the HS-142-1 treated group. 4.These findings support differential and selective responses of the three natriuretic peptides to AVO, in which plasma ANP and urinary CNP are markers for AVO. Secondly, these studies confirm the role of ANP and CNP but not BNP in the natriuretic and diuretic response to acute volume overload.


1994 ◽  
Vol 72 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Louise Béliveau ◽  
François Péronnet ◽  
Daniel G. Bichet ◽  
Réginald Nadeau

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.


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

Sign in / Sign up

Export Citation Format

Share Document