Possible Role for Atrial Natriuretic Peptide in Polyuria Associated With Paroxysmal Atrial Arrhythmias

Yamaji, Taiki; Ishibashi, Masayoshi; Nakaoka, Hidenori; Imataka, Kouji; Amano, Masao; Fujii, Jun

doi:10.1016/s0140-6736(85)92883-1

Cited by 158 publications

(36 citation statements)

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“…These findings suggest that ANP may play an important pathophysiol.ogical role in heart failure. It has been reported that plasma ANP levels are elevated in patients with supraventricular tachycardia (Schiffrin et al 1985 ;Tikkanen et al 1985 ;Yamaji et al 1985). In fact our patients with severe congestive heart failure also had supraventricular tachycardia.…”

Section: Discussionsupporting

confidence: 54%

“…There are three reports of elevated plasma ANP levels in paroxysmal aerial tachycardia (Schiffrin et al 1985;Tikkanen et al 1985;Yamaji et al 1985) and recently two reports have shown elevated plasma ANP levels in patients with congestive heart failure (Hartter et al 1985;Tikkanen et al 1985). However, it has not yet been elucidated whether ANP is released into the circulation in other diseases.…”

mentioning

confidence: 99%

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Plasma concentrations of atrial natriuretic peptide in various diseases.

Nozuki

Mouri

Itoi

et al. 1986

Tohoku J. Exp. Med.

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Section: Discussionsupporting

confidence: 54%

mentioning

confidence: 99%

Plasma concentrations of atrial natriuretic peptide in various diseases.

Nozuki

Mouri

Itoi

et al. 1986

Tohoku J. Exp. Med.

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“…9' 20 However, the protocol used in these latter studies did not permit one to determine whether the observed increase in plasma ANF was a direct effect of the exposure to high levels of neuromediators or whether it was an indirect effect of the concomitant changes in atrial wall tension. In this regard, a large number of experimental studies -4 7-9 and clinical observations5' 6, [10][11][12][13][14][15][16] clearly indicates that the level of atrial wall tension is a predominant factor in the regulation of ANF release. The experimental approach adopted in the present study represents a more physiologic attempt to study the peripheral effects induced by changes in eferent sympathetic discharge to the heart.…”

Section: Discussionmentioning

confidence: 99%

Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.

Volpe¹,

DeLuca²,

Atlas³

et al. 1988

Circulation

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The effects of endogenous activation of sympathetic nervous system on systemic and regional hemodynamics and on plasma levels of atrial natriuretic factor (ANF) were studied in subjects with essential hypertension. Stimulation of sympathetic nervous system was reflex-induced by a selective deactivation of carotid baroreceptors obtained by increasing external neck-tissue pressure (NTP) by means of a neck chamber. The effects of graded levels ( + 30, + 45, and + 60 mm Hg) and one single and sustained level ( + 45 mm Hg for 15 min) of NTP were studied. As expected, NTP caused reflex increases in blood pressure, heart rate, and forearm vascular resistance, whereas atrial pressures did not change significantly and cardiac output tended to increase. In the studies based on graded levels of NTP, immunoreactive ANF (irANF) progressively fell (from 31.7 + 10 to 13.3 + 4 fmol/ml; p < .05) and the changes in irANF were significantly correlated with those observed in FVR (r = -.671, p < .001). Both hemodynamic and irANF changes were prevented by adrenergic blockade (phentolamine + propranolol). During + 45 mm Hg NTP for 15 min, the levels of irANF fell both in the pulmonary artery and in the inferior vena cava. The irANF arteriovenous difference also fell during this maneuver. These data show that, in hypertensive patients, factors other than atrial wall tension may influence ANF release. They also show that endogenous sympathetic activation may reduce ANF release. Circulation 77, No. 5, 997-1002, 1988 A LARGE body of evidence indicates that the degree of atrial stretch or wall tension is a predominant factor in the regulation or atrial natriuretic factor (ANF) release in isolated heart preparations, 1, 2 intact animals,3 and human subjects.

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“…9,10) However, polyuria is not always observed during the paroxysms. Earlier studies reported that clinically detectable polyuria was observed only in 20 to 50% of patients with paroxysmal atrial fibrillation.…”

Section: Discussionmentioning

confidence: 99%

Distinct Increase in Hematocrit Associated with Paroxysm of Atrial Fibrillation

et al. 2000

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SUMMARYIn a previous study we found that hemoconcentration, which was identified by an increase in hematocrit, occured during a paroxysm of atrial fibrillation. In the present study we investigated the changes in hematocrit from sinus rhythm to paroxysm in 10 patients who had multiple paroxysms of atrial fibrillation in order to assess the ranges of the changes in hematocrit among the paroxysms. In these patients hematocrit was measured simultaneously with electrocardiographic recording during 3 or more paroxysms and sinus rhythm just before each paroxysm. The changes in hematocrit varied among the paroxysms. The maximum increase in hematocrit in each patient ranged from 3.5 to 8.0 points with an average of 5.1 points. Such a distinct increase in hematocrit which abruptly develops with a paroxysm of atrial fibrillation may be a potential risk for thrombus formation. (Jpn Heart J 2000; 41: 617-622)

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Possible Role for Atrial Natriuretic Peptide in Polyuria Associated With Paroxysmal Atrial Arrhythmias

Cited by 158 publications

References 6 publications

Plasma concentrations of atrial natriuretic peptide in various diseases.

Plasma concentrations of atrial natriuretic peptide in various diseases.

Reduction of atrial natriuretic factor circulating levels by endogenous sympathetic activation in hypertensive patients.

Distinct Increase in Hematocrit Associated with Paroxysm of Atrial Fibrillation

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