atrial-natriuretic-factor and Tachycardia--Paroxysmal

This article reviews the complex character of neuroendocrine response to paroxysmal tachycardia. While the endocrine influences in arrhythmogenesis are well perceived by the cardiologists, less attention has been paid to influence of tachycardia on neuroendocrine activation. However, this may significantly alter the clinical course of tachycardias and its responses to pharmacotherapeutic interventions. Main characteristics of hormones with direct relationship to cardiovascular system (ANP, AVP, catecholamines, angiotensin and others) are listed with description of regulation of their secretion and main biological effects, especially with regard to regulation of circulation. Changes in hemodynamics during tachycardia with accompanying changes in ANP, AVP renin-angiotensin-aldosterone system, sympatho-neural and sympatho-adrenal activation are reviewed. Further research and understanding require more complex approach and concentration on interrelationship of different regulatory hormones in tachycardia. (Fig. 2, Ref. 96.)

Topics: Atrial Natriuretic Factor; Cardiovascular Physiological Phenomena; Hemodynamics; Hormones; Humans; Neurosecretory Systems; Tachycardia, Paroxysmal

To estimate the influence of electrical cardioversion on the left ventricular systolic function, left atrial size, the plasma activity of creatinine phosphokinase (CPK) and its myocardial fraction (CK-MB) and plasma level of atrial natriuretic peptide (ANP) in patients with paroxysmal atrial fibrillation caused by coronary artery disease, hypertension or mitral valve disease.. The study underwent 36 patients with paroxysmal atrial fibrillation of mean duration 24.5 hours in which sinus rhythm was restored by electrical cardioversion.. Plasma activity of creatinine phosphokinase (CPK) and its myocardial fraction (CK-MB), plasma level of atrial natriuretic peptide (ANP) and echocardiographic examination were obtained before and 24 hour after electrical cardioversion. During echocardiographic examination were measured left ventricular end diastolic diameter (LVEDD), left ventricular ejection fraction (LVEF), left atrial size (LA) and early diastolic velocity(E) and velocity with atrial contraction (A) of left ventricular inflow. Electrical cardioversion was initiated with impulse of 100 J. If it failed to convert atrial fibrillation to sinus rhythm next impulse of 200 J and 360 J were consequently applied.. In all subgroups of patients formed dependently on a number of electrical shocks, 24 hour after cardioversion significant increase in left ventricular ejection fraction (LVEF) and decrease in plasma level of ANP were noted. In subgroup of patients treated with 1 (100 J) and 2 (100 + 200 J) impulse significant decrease in left atrial size was found out. The increase in plasma activity of creatinine phosphokinase (CPK) and its myocardial fraction (CK-MB) was confined to the subgroup treated with 3 (100 + 200 + 360 J) impulses. No changes in left ventricular end diastolic diameter (LVEDD) and early velocity (E) of left ventricular inflow 24 hours after cardioversion were observed. In all patients electrical cardioversion brought about the appearance of atrial wave of left ventricular inflow. No differences in estimated parameters between patients with coronary artery disease, hypertension and mitral valve disease were observed. Significant positive correlation between plasma level of ANP and left atrial size before (r = 0.69, p < 0.001) and after cardioversion (r = 0.68, p < 0.0001) were found.. Restoration of the sinus rhythm in patients with paroxysmal atrial fibrillation leads to the increase in left ventricular ejection fraction (LVEF) and to the decrease in left atrial size (LA) and the plasma level of atrial natriuretic peptide. Left atrial size and plasma level of ANP are related. The cardioversion with impulses of high energy increases the plasma activity of creatinine phosphokinase and its myocardial fraction.

Topics: Adult; Aged; Atrial Natriuretic Factor; Creatine Kinase; Electric Countershock; Female; Heart Atria; Humans; Isoenzymes; Middle Aged; Myocardium; Stroke Volume; Systole; Tachycardia, Paroxysmal; Ventricular Function, Left

Atrial natriuretic peptide (ANP) secretion increases after 30 min of paroxysmal supraventricular tachycardia (PSVT). Whether this phenomenon also applies to brain or C-type natriuretic peptides (BNP or CNP) remains unknown. Blood samples of 18 patients (41 ± 11 yr old; 4 men) with symptomatic PSVT and normal left ventricular systolic function (ejection fraction 65 ± 6%) were collected from the coronary sinus (CS) and the femoral artery (FA) before and 30 min after the induction, and 30 min after the termination of PSVT. The results showed that the ANP levels rose steeply after the PSVT and then reduced at 30 min after the termination (baseline vs. post-PSVT vs. posttermination: CS: 34.0 ± 29.6 vs. 74.1 ± 42.3 vs. 46.1 ± 32.9; FA: 5.9 ± 3.24 vs. 28.2 ± 20.7 vs. 10.0 ± 4.6 pg/ml; all P < 0.05). In contrast, compared with ANP, the increases of BNP and CNP in CS after the PSVT were less sharp, but continued to rise after the termination of tachycardia (BNP, 10.2 ± 6.4 vs. 11.3 ± 7.1 vs. 11.8 ± 7.9; CNP, 4.5 ± 1.2 vs. 4.9 ± 1.4 vs. 5.0 ± 1.4 pg/ml; all P < 0.05). The rise of BNP and CNP in FA was similarly less sharp after the PSVT and remained stationary after the termination. PSVT exerted differential effects on cardiac natriuretic peptide levels. ANP increased greater after a 30-min induced PSVT, but dropped faster after termination of PSVT, compared with BNP and CNP.

Topics: Adult; Atrial Natriuretic Factor; Biomarkers; Coronary Sinus; Disease Progression; Female; Femoral Artery; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Tachycardia, Paroxysmal; Tachycardia, Supraventricular; Time Factors

Topics: Adult; Age Factors; Area Under Curve; Atrial Fibrillation; Atrial Natriuretic Factor; Biomarkers; Case-Control Studies; Confidence Intervals; Diagnosis, Differential; Electrocardiography; Female; Hospitals, University; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Retrospective Studies; Risk Assessment; Singapore; Tachycardia, Paroxysmal

Natriuretic peptides (NPs) are excellent diagnostic and prognostic markers of heart failure, but their roles in atrial fibrillation (AF), particularly of isolated cardiac valvular origin, are unclear. We assessed the mRNA and protein content of pro-atrial natriuretic peptide (pro-ANP) and pro-brain natriuretic peptide (pro-BNP) in right atrial appendages (RAAs) and their N-terminal fragments (nt-proANP and nt-proBNP) in the plasma of 30 patients with paroxysmal AF (PaAF) and 40 patients with persistent AF (PeAF) matched with 34 patients in sinus rhythm (SR) undergoing isolated valvular replacement. To explore the underlying mechanism, fibrosis related examinations were simultaneously carried out in RAAs. Unexpectedly, atrial expression of pro-NPs mRNA was notably augmented in the PaAF subgroup, but not so pronounced in the PeAF subgroup. Atrial content of pro-NPs proteins and plasma nt-proNPs, between which surprisingly strong positive correlations were found (pro-ANP and nt-proANP: r=0.918, p<0.001; pro-BNP and nt-proBNP: r=0.913, p<0.001), were increased analogously in PaAF and PeAF subgroups. We identified significantly increasing gradients of atrial collagen volume fraction (CVF), levels of collagen I and III in the SR, PaAF and PeAF groups, and convincing negative linear correlations between CVF, levels of collagen I and III, and atrial transcripts of pro-NPs. These findings suggest that the discordance between transcripts and protein contents of pro-NPs was possibly due to the more outstanding atrial fibrosis in PeAF, and that circulating nt-proNPs levels could reflect the corresponding atrial pro-NPs contents in this report.

Topics: Adult; Atrial Appendage; Atrial Fibrillation; Atrial Function, Right; Atrial Natriuretic Factor; Collagen Type I; Collagen Type III; Female; Fibrosis; Gene Expression Regulation; Humans; Male; Middle Aged; Myocardium; Natriuretic Peptide, Brain; Natriuretic Peptides; Peptide Fragments; Protein Precursors; RNA, Messenger; Tachycardia, Paroxysmal

Radiofrequency (RF) catheter ablation has been shown to be highly effective in the treatment of supraventricular tachycardias. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (B-type natriuretic peptide; BNP) are secreted by the heart mainly in response to myocardial stretch induced by volume load. The aim of the present study was to determine the time course of the N-terminal prohormone forms of ANP (NT-proANP) and BNP (NT-proBNP) in patients undergoing radiofrequency (RF) catheter ablation for paroxysmal supraventricular tachycardias. Serial blood samples were taken from 13 patients with symptomatic paroxysmal supraventricular tachycardias undergoing RF ablation and from 13 age- and gender-matched healthy controls. Blood was taken before ablation (day 0, baseline), and at day one and day 120 after ablation. Levels of NT-proANP were significantly higher before RF ablation (4862+/-726 pmol/l) as compared to day one (2021+/-220 pmol/l) and day 120 after RF ablation (2470+/-349 pmol/l) (with p<0.01 on day one and p<0.05 on day 120; n=13). The size of the left atrium decreased from 41.0+/-5.5 mm before ablation to 34.9+/-5.9 mm (n=13; p<0.05) on day 120 as measured by M-mode echocardiography. Levels of NT-proBNP showed comparable values before and on day one and day 120 after ablation and were not significantly elevated as compared to healthy controls. NT-proANP levels are increased in patients presenting with paroxysmal supraventricular tachycardias and decrease one day after radiofrequency catheter ablation, possibly reflecting a transient reduction of ANP secretion from injured myocardial cells. Lower NT-proANP levels in the long-term time course may result from reduction of atrial volume load and reconstitution of atrial architecture after successful treatment of supraventricular tachycardias. NT-proANP may serve as a useful laboratory marker to describe the long-term interventional success after RF ablation.

Topics: Adult; Aged; Atrial Natriuretic Factor; Biomarkers; Catheter Ablation; Female; Humans; Male; Middle Aged; Predictive Value of Tests; Protein Precursors; Tachycardia, Paroxysmal; Tachycardia, Supraventricular

We sought to prospectively determine whether patients with congestive heart failure (CHF) at risk for paroxysmal atrial fibrillation (PAF) could be identified by clinical and study variables including the P-wave signal-averaged electrocardiogram (P-SAECG).. Although it is important to assess the risk of developing PAF in patients with CHF, it still remains difficult to predict the PAF appearance in patients with CHF clinically.. The study group consisted of 75 patients in sinus rhythm without a history of PAF, whose left ventricular ejection fraction, as measured by radionuclide angiography, was <40%. These patients underwent P-SAECG, echocardiography and 24-h Holter monitoring; in addition, the plasma concentration of atrial natriuretic peptide (ANP) was measured at study entry.. An abnormal P-SAECG was found at study entry in 29 of 75 patients. In the follow-up period of 21 +/- 9 months, the PAF attacks documented on the ECG significantly more frequently occurred in patients with (32%) rather than without an abnormal P-SAECG (2%) (p = 0.0002). The plasma ANP level was significantly higher in patients with rather than without PAF attacks (75 +/- 41 vs. 54 +/- 60 pg/ml, p = 0.01), although there were no significant differences in age, left atrial dimension or high grade atrial premature beats between the groups. The multivariate Cox analysis identified that the variables significantly associated with PAF development were an abnormal P-SAECG (hazard ratio 19.1, p = 0.0069) and elevated ANP level > or =60 pg/ml (hazard ratio 8.6, p = 0.018).. An abnormal P-SAECG and elevated ANP level could be predictors of PAF development in patients with CHF.

Topics: Adult; Aged; Aged, 80 and over; Atrial Fibrillation; Atrial Natriuretic Factor; Chromatography, High Pressure Liquid; Echocardiography; Electrocardiography, Ambulatory; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; Prognosis; Proportional Hazards Models; Prospective Studies; Radionuclide Ventriculography; Stroke Volume; Tachycardia, Paroxysmal

Patients with paroxysmal supraventricular tachycardia (SVT) may have a polyuria after termination of tachycardia. There is increasing evidence that the renal peptide urodilatin (ANP (95-126))--and not plasma ANP (ANP (99-126))--is the member of the natriuretic peptide family mediating natriuresis and diuresis in man. In patients with SVT we, therefore, analyzed the relationship between diuresis, natriuresis, plasma ANP, urinary urodilatin excretion and renal excretion of cyclic GMP, the second messenger in the ANP system. During and after clinical presentation with spontaneously occurring SVT, two patients with AV-nodal and one patient with atrioventricular reentry tachycardia (heart rate 160 to 200 bpm) were studied. Urinary urodilatin excretion was correlated to diuresis (r = 0.73) and natriuresis (r = 0.93); similarly urinary cyclic GMP excretion was related to diuresis (r = 0.80) and natriuresis (r = 0.87; p < 0.001, respectively). In contrast, there was no significant correlation between plasma ANP concentrations and diuresis (r = 0.28, n.s.) or natriuresis (r = 0.11, n.s.). As an explorative analysis, stepwise multiple linear regression identified urinary urodilatin as the most important contributor to diuresis and natriuresis after SVT. These data on polyuria after spontaneous SVT further support the view that in man urodilatin is the member of the natriuretic peptide family participating in kidney physiology.

Topics: Adult; Atrial Natriuretic Factor; Cyclic GMP; Diuresis; Female; Glomerular Filtration Rate; Humans; Male; Middle Aged; Natriuresis; Peptide Fragments; Polyuria; Regression Analysis; Tachycardia, Paroxysmal; Tachycardia, Supraventricular

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Dinoprostone; Female; Heart Rate; Humans; Kidney; Male; Middle Aged; Natriuresis; Osmolar Concentration; Polyuria; Tachycardia, Paroxysmal; Tachycardia, Supraventricular; Vasopressins

To assess the role of atrial natriuretic factor (ANF) in right ventricular (RV) infarction, 30 patients with inferior wall acute myocardial infarction (15 with RV involvement) and normal left heart filling pressures were studied 39 +/- 12 hours after the onset of symptoms. Serial measurements of cardiac output, right atrial, pulmonary artery and pulmonary wedge pressures, as well as plasma ANF, plasma renin activity, plasma aldosterone and vasopressin were obtained before and 30 minutes after acute volume expansion to raise wedge pressure greater than or equal to 20 mm Hg. Baseline mean right atrial pressure and plasma ANF levels were greater in patients with than without RV infarction (8 +/- 3 vs 5 +/- 2 mm Hg; p less than 0.0001, and 4.6 +/- 2.9 vs 2.7 +/- 1.5 fmol/ml; p less than 0.05, respectively). There were no differences in other baseline hemodynamic or humoral parameters between both groups. After volume expansion, pulmonary wedge pressure was similar in both groups, but right atrial pressure increased to higher levels in patients with RV infarction (19 +/- 2 vs 14 +/- 2 mm Hg; p less than 0.0001). Despite this greater stimulus for ANF secretion, the increase in plasma ANF was less pronounced in patients with RV infarction (63 +/- 81 vs 455 +/- 417%; p less than 0.002), especially among those with paroxysmal supraventricular tachyarrhythmias. Thus, despite higher baseline plasma levels of ANF, response to volume loading is markedly attenuated in patients with RV infarction complicating an inferior wall acute myocardial infarction.

Topics: Adult; Aged; Atrial Function; Atrial Natriuretic Factor; Female; Hemodynamics; Humans; Male; Middle Aged; Myocardial Infarction; Plasma Substitutes; Plasma Volume; Pulmonary Wedge Pressure; Tachycardia, Paroxysmal; Tachycardia, Supraventricular

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.

Topics: Animals; Atrial Function; Atrial Natriuretic Factor; Blood Pressure; Cardiac Output; Disease Models, Animal; Dogs; Heart; Heart Rate; Tachycardia, Paroxysmal

Atrial natriuretic peptide (ANP) is a cardiac hormone originating from atrial cardiocytes. It seems to be involved in the regulatory control of circulating volume and vascular tone. Plasma immunoreactive atrial natriuretic peptide (IrANP) was investigated in 22 patients with paroxysmal supraventricular tachyarrhythmia (16 with atrial fibrillation, 4 with atrial flutter, one with a Wolf-Parkinson-White syndrome (WPW) and one with atrial tachycardia). During the aute attack, IrANP was significantly increased (125.3 +/- 11.4 pmol/l) compared to samples obtained during convalescence (55.9 +/- 4.7 pmol/l). Heart rate (HR) was 144 +/- 4.3 beats/min during the arrhythmia and 75 +/- 2.6 during convalescence. The reduction of IrANP in plasma from the acute attack of tachycardia to follow-up was significantly related to the reduction of HR (p less than 0.05). Irrespective of type of paroxysmal supraventricular tachyarrhythmia, 50% of the patients experienced polyuria during the attack. This symptom was more frequent in younger patients with a shorter duration of tachycardia. Polyuria patients had a higher HR during the attack of supraventricular tachycardia. Even though polyuria was not always found in the patients with the highest IrANP values, the symptom was associated with significantly higher concentrations of IrANP in plasma compared to the non-polyuria group. We conclude that IrANP is increased in plasma during acute attacks of paroxysmal supraventricular tachycardia. Furthermore, the polyuria frequently associated with this condition may partly be due to excess release of ANP from cardiac myocytes.

Topics: Adult; Aged; Atrial Natriuretic Factor; Humans; Middle Aged; Polyuria; Radioimmunoassay; Tachycardia, Paroxysmal; Tachycardia, Supraventricular

To examine the interrelationship between human atrial natriuretic polypeptide (hANP) and cyclic 3'5'-guanosine monophosphate (cyclic GMP), plasma concentrations of these compounds were determined in 61 disease-free humans, as controls, and in 35 patients with congestive heart failure. Levels of plasma hANP (199.6 +/- 53.7 pg/ml) and cyclic GMP (12.6 +/- 1.7 pmol/ml) in patients with congestive heart failure were significantly higher than in the control subjects (hANP 57.1 +/- 2.8 pg/ml, cyclic GMP 5.2 +/- 0.3 pmol/ml). Although plasma hANP concentrations in the patients with congestive heart failure tended to increase with the severity of cardiac dysfunction, there was no significant correlation between the levels of plasma hANP and the grade of heart failure, classified according to the New York Heart Association. However, a significant correlation was found between plasma hANP and cyclic GMP concentrations in both the healthy subjects and the patients with congestive heart failure, and a weak positive correlation between plasma hANP and cyclic 3'5'-adenosine monophosphate (cyclic AMP) concentration in the patients with congestive heart failure. Thus, changes in plasma cyclic GMP concentration depend to some extent on the plasma concentrations of hANP.

Topics: Adult; Aged; Atrial Natriuretic Factor; Cyclic AMP; Cyclic GMP; Heart Failure; Humans; Middle Aged; Tachycardia, Paroxysmal

To investigate the mechanisms of polyuria associated with tachycardia, we measured plasma concentrations of alpha-human atrial natriuretic polypeptide (alpha-hANP) and cGMP in 6 patients with paroxysmal tachycardia. Plasma concentrations of immunoreactive alpha-hANP and cGMP increased by +69% (p less than 0.05) and +100% (p less than 0.05), respectively, during both paroxysmal atrial tachycardia and atrial fibrillation. To examine whether tachycardia per se raises the secretion of alpha-hANP, we also determined plasma concentrations of alpha-hANP and cGMP in 5 patients during rapid atrial pacing. The pacing-induced tachycardia also increased both of the plasma concentrations. Further, the examinations of cardiac and renal functions in patients with complete atrioventricular block during rapid pacing revealed that each of the increases in atrial pressures, urinary sodium excretion and creatinine clearance were in parallel with the change in plasma concentration of alpha-hANP. These results suggest that an increase in plasma concentration of alpha-hANP during paroxysmal tachycardia is mainly due to elevation of atrial pressure and that this increase in alpha-hANP contributes to tachycardia polyuria.

Topics: Atrial Fibrillation; Atrial Natriuretic Factor; Cardiac Pacing, Artificial; Cyclic GMP; Heart; Heart Block; Humans; Kidney; Middle Aged; Radioimmunoassay; Tachycardia, Paroxysmal; Time Factors

Plasma concentrations of antidiuretic hormone (ADH) were measured in 8 patients with congestive heart failure (CHF) of NYHA functional class III-IV, before and during treatment with captopril, 6.25-25.0 mg t.i.d., added to their drug regimen. Before captopril treatment, plasma ADH was high, 2.5 times the upper limit of normal reference values. During treatment with captopril, plasma ADH levels were normalized, and remained so throughout the study, for at least 6 months. Plasma levels of angiotensin II were also reduced to a normal level. Reduction of plasma ADH during captopril treatment in CHF may partly depend on reduced angiotensin II formation, and may be beneficial by improving water balance. Atrial natriuretic peptide (ANP), was measured by radioimmunoassay in 17 patients with CHF. The highest levels were measured in the most severe CHF cases, and intermediate high values on NYHA functional class I-II patients. Plasma ANP concentrations in control patients (n = 18) without cardiac diseases ranged between 0 and 30 pg/ml. In two patients with paroxysmal supraventricular tachycardia, associated with transient polyuria, high plasma ANP concentrations were noticed during tachycardic episodes. Thus, ANP appears to be a circulating hormone in humans, and is released into the blood in clinical conditions associated with raised preload and atrial wall stretch.

Topics: Aged; Aldosterone; Angiotensin II; Atrial Natriuretic Factor; Captopril; Female; Heart Failure; Humans; Male; Middle Aged; Renin; Tachycardia, Paroxysmal; Vasopressins

The human atrial natriuretic polypeptide (hANP) concentration in plasma was measured during paroxysmal supraventricular tachycardia provoked in 2 patients with Wolff-Parkinson-White syndrome. A 10- to 20-fold increase in plasma hANP concentration was observed during the tachycardia: from 12 to 291 pg/ml in 1 case and from 14 to 174 pg/ml in the other. Although polyuria was associated with the tachycardia, urinary sodium excretion as well as urinary osmolality were decreased. The urinary arginine vasopressin was appreciably decreased during the tachycardia. These results suggest that hANP released by paroxysmal tachycardia might not act as a natriuretic factor in this range of plasma concentration. Polyuria during paroxysmal tachycardia was attributed mainly to the inhibition of arginine vasopressin release.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Electric Stimulation; Female; Heart; Humans; Male; Middle Aged; Polyuria; Tachycardia, Paroxysmal; Wolff-Parkinson-White Syndrome

Topics: Aged; Atrial Natriuretic Factor; Female; Humans; Middle Aged; Muscle Proteins; Tachycardia, Paroxysmal

Plasma concentrations of immunoreactive atrial natriuretic peptide (ANP) were low or undetectable in 8 healthy subjects and 9 control patients without cardiac disease, and raised in 17 patients with congestive heart failure (CHF). Highest concentrations were measured in patients with severe CHF. High plasma ANP levels were also found in 2 patients with paroxysmal supraventricular tachycardia and associated transient polyuria. Infusion of synthetic human alpha-ANP, 110-125 micrograms over 30 min, to 3 healthy males resulted in a 2.3-fold increase in natriuresis and diuresis but had no effect on kaliuresis. Plasma levels of renin activity, aldosterone, and antidiuretic hormone did not change significantly. ANP infusion gave plasma ANP levels of the same magnitude as those found in severe CHF; levels returned to baseline within 15 min of stopping the infusion. Thus ANP appears to be a circulating hormone in man, at least in severe CHF and supraventricular tachycardia.

Topics: Adult; Aged; Atrial Natriuretic Factor; Blood Pressure; Female; Heart Failure; Heart Rate; Hormones; Humans; Infusions, Parenteral; Male; Middle Aged; Muscle Proteins; Polyuria; Tachycardia, Paroxysmal

Topics: Adult; Atrial Natriuretic Factor; Female; Humans; Muscle Proteins; Natriuresis; Tachycardia, Paroxysmal