Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia.

Abstract

tion, however, was not available for other causes of death. In the process of random sampling mostly interior villages were chosen, where qualified medical practitioners were generally not available.A shortcoming of the present analysis may be that the mortality rates were not adjusted for socioeconomic status. Nevertheless, only a small percentage of the target population could be classed as not being poor and therefore, unless the numbers in some categories are small, the confounding effect (if any) would not cause any appreciable difference. The numbers were small for tobacco chewers and multiple users for men and chewing and other usage for women.Bidi smoking and chewing tobacco with betel leaf are known to carry a 30-500 o higher risk of mortality.4 5 Thus tobacco usage appears to be injurious to health in any form and more so in the form of rnverse chutta smoking. Mechanism of polyuria and natriuresis in atrioventricular nodal tachycardia R CANEPA-ANSON, M WILLIAMS, J MARSHALL, T MITSUOKA, S LIGHTMAN, R SUTTON Abstract A woman with tachycardia associated with polyuria was investigated. Electrophysiological analysis showed that the tachycardia was an atrioventricular nodal re-entrant tachycardia. Programmed stimulation was then used to provoke and sustain the tachycardia for 40 minutes. Polyuria, with an appreciable increase in free water clearance, was observed. This was associated with reduction in plasma and urinary arginine vasopressin concentrations. Appreciable natriuresis also developed.These results support the hypothesis that the polyuria with increased free water clearance and the natriuresis occurring during sustained tachycardia in man are due to inhibition of secretion of vasopressin and the release of natriuretic factor. IntroductionThe association between paroxysmal tachycardia and polyuria is well recognised and has been reported to occur in 20%, to 50%/ of patients with these arrhythmias.' 2 Neither the reason

Plasma Atrial Natriuretic Polypeptide and Polyuria during Paroxysmal Tachycardia in Wolff-Parkinson-White Syndrome Patients

“…Lang et al [4] reported that volume loading in rats produced a rise in plasma ANP-like material with an elevation in atrial pressure. The present study supports this finding, since it has been shown that paroxysmal tachycardia elevates left atrial pressure [8]. Whether the tachycardia itself has stimulating effects on the secretion of hANP remains to be determined.…”

“…Natriuresis as well as polyuria have been attributed to the release of hANP [8]. Conversely, we found a decrease in sodium excretion during the tachycardia.…”

“…However, it is possible that drastic circulatory changes caused by the paroxysmal tachycardia [5] have negated the natriuretic activity of hANP. Polyuria associated with paroxysmal atrioventricular nodal tachycardia may be a reflex inhibi tion of the AVP release generated by the rise in atrial pressure [8]. The same could also be said for the tachy cardia of WPW syndrome, since urinary osmolality and AVP excretion were decreased during the tachycardia, compared with the control period.…”

“…Paroxysmal tachycardia is accom panied by polyuria in 50% of the cases [5,6]. The mecha nism of polyuria is assumed to be a reflex inhibition of arginine vasopressin (AVP) release by an elevation in atrial pressure [7], Canepa-Anson et al [8] have con firmed this thesis in a patient by provoking paroxysmal atrioventricular nodal tachycardia. Moreover, they found natriuresis as well as polyuria during the tachy cardia and attributed these events to the release of hANP.…”

Effects of Anticoagulation Intensity on Hemostatic Markers in Patients With Non-Valvular Atrial Fibrillation

“…12 Hemoconcentration is one of the major mechanisms for the development of stroke and is induced by paroxysmal AF, probably because of increased secretion of atrial natriuretic peptide and decreased secretion of vasopressin. 22,23 The concentrations of hemostatic markers in patients with paroxysmal AF may vary depending on the frequency and duration of the AF episodes in each patient. Therefore, a lower anticoagulation intensity would not be recommended for the prevention of ischemic stroke in patients with paroxysmal AF as compared with patients with chronic AF.…”