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Year : 1984  |  Volume : 30  |  Issue : 4  |  Page : 255-6

The possible role of natriuretic hormone in idiopathic oedema and mitral valve prolapse--a hypothesis.







How to cite this article:
Vaidya A B. The possible role of natriuretic hormone in idiopathic oedema and mitral valve prolapse--a hypothesis. J Postgrad Med 1984;30:255


How to cite this URL:
Vaidya A B. The possible role of natriuretic hormone in idiopathic oedema and mitral valve prolapse--a hypothesis. J Postgrad Med [serial online] 1984 [cited 2019 Nov 21];30:255. Available from: http://www.jpgmonline.com/text.asp?1984/30/4/255/5433



Idiopathic oedema (I.O.) is a chronic disorder of uncertain etiology and it seldom remits.[4],[7] Mitral valve prolapse (M.V.P.) is one of the most frequently observed cardiac abnormalities.[8] M.V.P. is, like I.O., a familial disorder that occurs more frequently in females.[8] The coexistence of these two conditions in a patient prompted the unitary hypothesis that "a deficiency of natriuretic hormone may explain the pathophysiological basis of some of the symptoms of both these disorders".
The patients with I.O. and with M.V.P. feel better while supine and develop ill defined malaise, fatigue and edema during orthostasis. In M.V.P., standing, sitting, tachycardia, amyl nitrite and isoprenaline decrease the left ventricular volume whereas squatting, supine position, bradycardia, propranolol and some vasopressors have the opposite effect. All the measures which tend to increase the preload also reduce the symptoms of M.V.P. and vice versa.[8] In patients with I.O. too, supine position, propranolol etc., have been claimed to be of a symptom relieving value.[7] These observations suggest a possibility that a decreased left atria( blood volume may trigger the symptoms by a reduction in the synthesis or release of the atrial natriuretic hormonal peptide.
Redistribution of the normal blood volume from the peripheral to the central compartment is known to induce natriuresis. In a normal man, immersion in water upto the neck leads to natriuresis.[2] Similarly, a study in conscious dogs has revealed that a reversible partial occlusion of the mitral valve leading to an elevation of the left atrial pressure causes "atrial natriuresis".[6] During orthostasis with a diminished venous return, there would be a decrease in the left atrial volume and pressure; this would be greater still with a floppy mitral valve. A consequently diminished stretch of the left atrial wall would provide a signal for a reduction in the synthesis and release of the natriuretic peptide. This would result in reduced circulating levels of the natriuretic hormone, with the following consequences: (a) greater retention of sodium and fluid, leading to edema and (b) peripheral vasodilatation due to diminished inhibition of the vascular Na+K+ATPase.[3] These factors would further reduce the venous return and the preload. Under these conditions, a symptomatic patient of I.0. or M.V.P. would feel better when she/he lies down.
It is of interest to note that in hypertension, contrary to the aforesaid hypertension, an increase in the natriuretic factor has been demonstrated to play a pathogenetic role.[1],[5]
The presence of idiopathic postural hypotension in some patients of I.0. or M.V.P. also is a coroborating piece of evidence for the present hypothesis. We are currently engaged in investigating the patients of I.0., M.V.P. and orthostatic hypotension to refute or validate the hypothesis.

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1.de Wardener, H. E.: Natriuretic hormone. Clin. Sci. Mol. Med., 52: 1-8, 1977.   Back to cited text no. 1    
2.Epstein, M., Bricker, N. S. and Bourgoignie, J. J.: Presence of a natriuretic factor in urine of normal man undergoing water immersion. Kidney Internat., 13: 152-158, 1978.  Back to cited text no. 2    
3.Gonick, H. C., Kramer, H. J., Paul, W. and Lu, E.: Circulating inhibitor of sodium-potassium activated adenosne triphosphatase after expansion of extracellular fluid volume in rats. Clin. Sci. Mol. Med., 53: 329-334, 1977.  Back to cited text no. 3    
4.Khokhani, R. C., Vaidya, A. B. and Sheth, U. K.: Idiopathic oedema. Ind. J. Med. Sci., 21: 831-832. 1967.  Back to cited text no. 4    
5.MacGregor, G. A., Fenton, S., Alagha-band-Zadeh, J., Markandu, N., Roubston, J. E. and deWardener, H. E.: Evidence for a raised concentration of a circulating sodium transport inhibitor in essential hypertension, Brit. Med., J., 283: 1355-1357, 1981.  Back to cited text no. 5    
6.Reinhardt, H. W., Kakezmarczyk, G., Mohnhaupt, R. and Simge, B.: The possible mechanism of atrial natriuresis; Experiments on chronically instrumented dogs. In, "Hormonal Regulation of Sodium Excretion." Editors: B. Lichardus, R. W. Schrier and J. Power, Elsevier/North Holland Biomedical Press, Amsterdam, 1980, pp. 263-272.  Back to cited text no. 6    
7.Streeten, D. H. P.: Idiopathic edema. In, "Current Therapy in Endocrinology 1983-1984." Editors: Dorothy J. Krieger and C. Wayne Baldin, The C. V. Mosby Company, Saint Louis, 1983, pp. 150-153.   Back to cited text no. 7    
8.Tesch, D. D. and Siege!, R.: "Primary Cardiology." P. W. Communications, November-December: 10, 1976.  Back to cited text no. 8    

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Online since 12th February '04
2004 - Journal of Postgraduate Medicine
Official Publication of the Staff Society of the Seth GS Medical College and KEM Hospital, Mumbai, India
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