Effects of endogenous atrial natriuretic peptide released by rapid atrial pacing in dogs

1987 ◽  
Vol 253 (4) ◽  
pp. R599-R604 ◽  
Author(s):  
K. P. Walsh ◽  
T. D. Williams ◽  
R. Canepa-Anson ◽  
E. Pitts ◽  
S. L. Lightman ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Atrial Pacing ◽  
Vascular Effects ◽  
Rebound Increase ◽  
Atrial Natriuretic

The relationships between the hemodynamic, renal, and endocrine changes induced by rapid atrial pacing were studied in seven chloralose-anesthetized greyhounds paced from the right atrial appendage for 60 min at 250 beats/min. Pacing increased mean pulmonary wedge pressure, decreased cardiac output, and decreased mean arterial pressure. Systemic vascular resistance did not change significantly. Coronary sinus atrial natriuretic peptide (ANP) concentrations rose maximally within 5 min of commencing pacing. The corresponding increase in arterial ANP concentrations during this time was only 44% of its maximum value after 30 min of pacing. Plasma concentrations of arginine vasopressin were unchanged. Plasma renin activity decreased during pacing and showed a marked rebound increase at 60 min postpacing. Plasma norepinephrine levels did not change significantly during pacing. Urine flow increased during the latter 30 min of pacing. There was no significant change in sodium clearance despite high sustained concentrations of ANP. The lack of significant natriuretic and systemic vasodilator effects in association with high arterial plasma concentrations of endogenous ANP, in the absence of antagonistic mechanisms, suggests that the natriuretic and vascular effects of ANP may not be its major physiological actions.

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.

Inhibition of Plasma Renin Activity (PRA) by Physiological Plasma Concentrations of Atrial Natriuretic Peptide (ANP) in Man

1987 ◽  
Vol 72 (s16) ◽  
pp. 63P-63P
Author(s):  
J V Anderson ◽  
J Donckier ◽  
N N Payne ◽  
J Breckwoldt ◽  
J D H Slater ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Renin Activity ◽  
Atrial Natriuretic

Atrial natriuretic peptide: Evidence of action as a natriuretic hormone at physiological plasma concentrations in man

1987 ◽  
Vol 72 (3) ◽  
pp. 305-312 ◽  
Author(s):  
J. V. Anderson ◽  
J. Donckier ◽  
N. N. Payne ◽  
J. Beacham ◽  
J. D. H. Slater ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Natriuretic Hormone ◽  
Plasma Aldosterone Concentration ◽  
Water Excretion ◽  
Physiological Range ◽  
Atrial Natriuretic

1. The administration of exogenous atrial natriuretic peptide (ANP) causes a natriuresis and diuresis in man, but this has, to date, only been demonstrated at plasma ANP concentrations within the high pathological or pharmacological ranges. Evidence that ANP acts physiologically requires the demonstration of a natriuretic effect when it is infused to recreate plasma concentrations similar to those observed after physiological stimuli. 2. We infused human α-ANP (1–28) at a calculated rate of 1.2 pmol min−1 kg−1 for 3 h into seven water-loaded normal subjects, achieving plasma ANP concentrations within the upper part of the physiological range. The subjects' resting plasma ANP concentration increased from 3.8 ± 1.5 to 20.9 ± 1.9 pmol/l. 3. The infusion of ANP caused a 60% increase of mean urinary sodium excretion from 111 ± 18 to 182 ± 30 μmol/min (P < 0.001) and a 28% increase of mean water excretion from 10.8 ± 0.8 to 13.8 ± 1.6 ml/min (P < 0.01). 4. The infusion suppressed mean plasma renin activity from 1.55 ± 0.10 to 1.17 ± 0.06 pmol of ANG I h−1 ml−1 (P < 0.001). Mean plasma aldosterone concentration (242 ± 16 basally and 215 ± 15 pmol/l at the end of ANP infusion) did not change significantly. Pulse rate and blood pressure were unchanged throughout the study. 5. No significant change in any of the variables mentioned above occurred during the infusion of the vehicle alone on a separate study day. 6. The demonstration that recreation of plasma concentrations of ANP within the physiological range by intravenous infusion induces a natriuresis provides new evidence supporting the role of ANP as a natriuretic hormone.

Atrial natriuretic peptide released by rapid ventricular pacing in dogs does not cause a natriuresis

1988 ◽  
Vol 74 (6) ◽  
pp. 571-576 ◽  
Author(s):  
K. P. Walsh ◽  
T. D. M. Williams ◽  
R. Canepa-Anson ◽  
P. Roe ◽  
E. Pitts ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Free Water ◽  
Right Atrial ◽  
Ventricular Pacing ◽  
Free Water Clearance ◽  
Rapid Ventricular Pacing ◽  
Sodium Clearance ◽  
Atrial Natriuretic

1. The relationships between the haemodynamic, renal and endocrine changes induced by rapid ventricular pacing were studied in ten chloralose-anaesthetized dogs paced from the right ventricular apex for 60 min at 250 beats/min. 2. Pacing increased mean right atrial and mean pulmonary wedge pressure (P < 0.05), and decreased cardiac output and mean arterial pressure (P < 0.05). 3. Coronary sinus atrial natriuretic peptide (ANP) concentrations were approximately fourfold greater than arterial concentrations; both increased markedly during pacing (P < 0.01). Plasma concentrations of arginine vasopressin and plasma renin activity did not change signficantly. 4. Urine flow and free water clearance increased during the latter 30 min of pacing (P < 0.05). There was no significant change in sodium clearance despite high sustained concentrations of ANP. 5. Without the availability of specific inhibitors of ANP release or action, we are unable to exclude the possibility that ANP may have prevented sodium clearance from otherwise decreasing during rapid ventricular pacing. Nevertheless, the dissociation between elevated ANP concentrations and natriuresis in this study indicates that a rise in ANP concentrations per se is not sufficient to produce a natriuresis.

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.

Atrial natriuretic peptide inhibits postural release of renin and vasopressin in humans

1988 ◽  
Vol 255 (3) ◽  
pp. R368-R372 ◽  
Author(s):  
T. D. Williams ◽  
K. P. Walsh ◽  
S. L. Lightman ◽  
R. Sutton
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Volume ◽  
Plasma Renin ◽  
The Other ◽  
Plasma Norepinephrine ◽  
Head Up Tilt ◽  
Plasma Arginine ◽  
Rate Infusion ◽  
Atrial Natriuretic

The effects of infusions of atrial natriuretic peptide (ANP) on the hormonal and hemodynamic responses to head-up tilt were investigated in six healthy adults. Head-up tilt at 45 degrees for 2 h during placebo saline infusion caused a 7% fall in blood volume accompanied by increases in plasma renin activity (PRA) and plasma arginine vasopressin (AVP) of 112 and 175%, respectively. Head-up tilt was repeated during an infusion of ANP producing a four- to sixfold increase in plasma ANP concentrations. This resulted in an 18% fall in plasma volume, yet despite this greater fall in plasma volume, PRA did not change. Two subjects experienced vasovagal symptoms toward the end of the ANP infusions accompanied by large increases in plasma AVP. In the other four subjects, plasma AVP remained unchanged during ANP infusions. Both procedures resulted in similar increases in plasma norepinephrine levels and in heart rate. Infusion of ANP prevents the posturally stimulated release of renin and AVP.

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.

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