Atrial Natriuretic Peptide Release is Determined by Atrial Pressure and Not Heart Rate

1987 ◽  
Vol 73 (s17) ◽  
pp. 56P-56P
Author(s):  
K P Walsh ◽  
T D M Williams ◽  
C Spiteri ◽  
E Pitts ◽  
S L Lightman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Peptide Release ◽  
Atrial Natriuretic

Paradoxical inhibition of atrial natriuretic peptide release during pacing-induced hypotension

1987 ◽  
Vol 73 (5) ◽  
pp. 459-462 ◽  
Author(s):  
P. Erne ◽  
A. E. G. Raine ◽  
E. Burgisser ◽  
E. Gradel ◽  
F. Burkart ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Catecholamines ◽  
Cardiac Pacing ◽  
Systemic Blood Pressure ◽  
Atrial Pressure ◽  
Ventricular Pacing ◽  
Peptide Release ◽  
Atrial Natriuretic

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.

Effect of Right Atrial Stimulation on both Atrial Pressure and Atrial Natriuretic Peptide Release in Essential Hypertension

Cardiology ◽  
1991 ◽  
Vol 78 (4) ◽  
pp. 304-310 ◽  
Author(s):  
A. Michelucci ◽  
L. Padeletti ◽  
A. Monopoly ◽  
G. Fabbri ◽  
C. Tostiguerra ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Peptide Release ◽  
Atrial Stimulation ◽  
Atrial Natriuretic

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.

Relationship between status of plasma atrial natriuretic peptide and heart rate variability in human subjects

2012 ◽  
Vol 28 (2) ◽  
pp. 208-214 ◽  
Author(s):  
Yuji Kasamaki ◽  
Yoichi Izumi ◽  
Yukio Ozawa ◽  
Masakatsu Ohta ◽  
Ayako Tano ◽  
...  
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Human Subjects ◽  
Plasma Atrial Natriuretic Peptide ◽  
Atrial Natriuretic

Potentiation of stretch-induced atrial natriuretic peptide secretion by intracellular acidosis

1999 ◽  
Vol 277 (1) ◽  
pp. H405-H412 ◽  
Author(s):  
Pasi Tavi ◽  
Mika Laine ◽  
Sari Voutilainen ◽  
Petri Lehenkari ◽  
Olli Vuolteenaho ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Imaging System ◽  
Atrial Pressure ◽  
Intracellular Acidosis ◽  
Contraction Force ◽  
Atrial Contraction ◽  
Intracellular Ca ◽  
Peptide Secretion ◽  
Atrial Natriuretic

We sought to investigate whether atrial myocyte contraction and secretion of the atrial natriuretic peptide (ANP) are affected in the same manner by intervention in intracellular Ca2+ handling by acidosis. The effects of propionate (20 mM)-induced intracellular acidosis on the stretch-induced changes in ANP secretion, contraction force, and intracellular Ca2+ concentration ([Ca2+]i) were studied in the isolated rat atrium. The stretch of the atrium was produced by increasing the intra-atrial pressure of the paced and superfused preparation. Contraction force was estimated from pressure pulses generated by the contraction of the atrium. Intracellular Ca2+ was measured from indo 1-AM-loaded atria, and ANP was measured by radioimmunoassay from the perfusate samples collected during interventions. Intracellular pH of the atrial myocytes was measured by a fluorescent indicator (BCECF)-based imaging system. Intracellular acidification caused by 20 mM propionic acid (0.18 pH units) potentiated the stretch-induced (intra-atrial pressure from 1 to 4 mmHg) ANP secretion, causing a twofold secretion compared with nonacidotic controls. Simultaneously, the responsiveness of the atrial contraction to stretch was reduced ( P < 0.05, n = 7). Stretch augmented the systolic indo 1-AM transients in acidic ( P < 0.05, n = 6) and nonacidic atria ( P < 0.05, n = 6). However, during acidosis this was accompanied by an increase of the diastolic indo 1-AM ratio ( P < 0.05, n = 6). Cooccurrence of stretch and acidosis caused an increase in systolic and diastolic [Ca2+]i and potentiated the stretch-induced ANP secretion, whereas the contraction force and its stretch sensitivity were decreased. This mechanism may be involved in ischemia-induced ANP secretion, suggesting a role for ANP secretion as an indicator of contractile dysfunction.

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