Arendt, Rainer M.

Gerbes, Alexander L.

Knorr, H. J.

Lindner, Jörg

Schnizer, W.

Schöps, P.

English

Open Access LMU

P M R V O L 3 N O 3 1 9 9 1 From the *Department of Physical Medicine, the **Department of Medicine I, and the ***Department of Medicine II, Klinikum Grqßhadern, University of Munich The Effect of Different Water Temperatures on the Release of the Atrial Natriuretic Factor (ANF) During 'Head Out Water Immersion (HOI)" W. Schnizer*, H. Knorr*, A.L. Gerbes***, R.M. Arendt**, J. Lindner* and P. Schöps* Key-words: Physiology of water immersion - endocrine reaction in hot environment - atrial natriuretic factor Summary: Head-out water immersion (HOI) results in a redistribution of blood volume with a relative central hypervolemia, which is the cause of increased secretion of the atrionatriuretic factor (ANF). This study was conducted to examine the role of different bath temperatures for the stimulation of ANF secretion. Twelve healthy subjects were immersed in 4 water baths (24, 28. 35 and 39 *C) for 40 min in a randomized fashion. Plasma ANF was determined by radioimmunoassay following extraction. The baths led to a significant increase in plasma ANF. Maximal increments were the highest in hot baths. This data suggests that heat induced changes in circulation may modulate the secretion of ANF. The importance of heart rate is being discussed. The atrial natriuretic factor (ANF) is a polypeptide which is synthe­sized and stored in the secretarial granula of the atria (1). It probably also affects the regulation of the extracellular water balance and blood pressure, without a final ex­planation of its physiological sig­nificance. Hypervolemia is one of the most important factors for the release of the hormone (2). In addition water immersion has effects on blood volume and many other physiological reactions (3). An important consequence of the hydrostatic pressure is a change in the blood volume distribution within the low pressure system with preference on the in­trathoracic vascular system. Cen­tral blood volume and central venous pressure increase, it is therefore not surprising that HOI Prof. Dr. W. SCHNITZER, Privatklinik Raphael, Am Kurwald 10, A-8394 Bad Griesbach, Austria results in ANF release into the cir­culation (4-9). Water immersion has proved to be a valid model for the study of blood volume regulation and is generally carried out with thermoneutral temperatures (about 34r-36 #C). Yet there are varying water tem­peratures with different forms of therapeutical baths, which can af­fect significant cardiovascular, hormonal and metabolic reactions and may influence the conditions of ANF-secretion by changing the central haemodynamics. There­fore we investigated the effects of cool and hot baths on plasma con­centration of ANF. Methods The study included 12 healthy subjects (4 females, 8 males with mean age of 26 ± 2 years). They had no specific nutrition. In­formed consent was obtained in respect to the conditions of the declaration of Helsinki. In a randomized fashion the sub­jects took four baths (HOI) with a one week interval; temperatures were 24, 28, 35 and 39 *C respec­tively. A sitting position was kept for 40 minutes before - during -and after the baths. The experi­ments were carried out in the af­ternoon. The subjects had to drink 150 ml of water per hour in order to guarantee a standardized hy­dration. Venous blood samples were drawn before 10,20 and 40 minutes after the start as well as 20 and 40 min­utes after the end of immersion. The blood samples were immedi­ately transferred into precooled containers (1 mg/ml Na-EDTA, 500 KIV/ml Aprotinin); the plas­ma was deep-frozen at -80 *C after centrifugation. ANF was deter­mined with a RIA within extracted plasma (10). In addition heart rate, blood pressure and sublin­gual temperatures were regis­tered. The paired t-test was used for sta­tistical evaluation of changes in plasma ANF. Values of ρ < 0.05 were considered significant. P M R V O L 3 N O 3 1 9 9 1 Results The mean values of ANF measure­ments for different baths are shown in Figure 1 onapercentba-sis. The single values before and after the baths ranged from 1.9-8.4 (x = 4.7 ± 0.25) respectively 2.&-17.2 (x = 7.1 ± 0.68) f mol/ml plasma. In all the series there was an increase in ANF concentration in the blood as a result of water im­mersion. At the end of the water immersion (40 min) there were veiy similar values for the groups of 24, 28 and 35 9C. Differences during the time course were not significant. There was a stronger secretion of ANF in the hyperthermic bath (39 *C). Already after 20 minutes a significantly higher concentration was observed in comparison to the other groups. After 40 minutes 224% of the initial value were achieved, which equals three times the value of the ther-moneutral immersion values. The ANF levels quickly decreased after ending the immersion phase, al­though not achieving the basal values after 40 minutes. Haemodynamics as well as sublin­gual temperatures showed the fol­lowing changes: In cool baths (24 and 28 *C) there was a slight in­crease in blood pressure and de­crease of heart rate as well as a reduction of the sublingual tem­peratures (1.1 resp. 0.6 *C). The hot baths (39 VC) led to a decrease of the diastolic blood pressure and an elevation of heart rate from 74 up to 103 min-1; the sublingual temperature increased by 1 *C. Discussion The increased hydrostatic pres­sure during water immersion (HOI) on the peripheral vessels leads to a preferential distribution of the blood volume into the cen­tral intrathoracic vessels. This im­mersion related central hypervolemia results from an in­crease of blood volume of about 700 ml of blood and increases the central venous pressure by ap­proximately 15 mm Hg (3). This led to a stimulus in the regulation of the extracellular fluid volume (11). The atrial natriuretic factor (ANF) is known to be a hormone for blood volume control. Experiments have proved the expansion of blood vol­ume with an increase of the right atrial pressure causing a release of ANF into the circulation (2). For this reason tension stimuli of the atrial muscle might be the trigger­ing factor. In addition heart rate is also con­sidered to be important (12-14). The increase of central venous pressure during water immersion results in an acute volume stress. Under these circumstances a rein­forced release of ANF has been proved. An increase in plasma concentration of 27% within 10 minutes was found by Gerbes et al. (6, 7). Anderson et al. (4), Ep­stein et al. (5), Ogihara et al. (8) and Pendergasttt al. (9) confirmed the effects of water immersion on ANF. Differences in thermoneutral wa­ter temperatures may show var­ious thermophysiological responses depending on intensity and dura­tion of exposition. Hot and cold stimuli especially show an imme­diate reaction on haemodynam­ics, metabolic and endocrine functions. The release of ANF could be influenced under these circumstances. Exposition to cold leads to an in­crease of mean arterial blood pres­sure as a consequence of complex circulatory regulation with pe­ripheral vasoconstriction and an increase of vascular total periph­eral resistance (TPR). Our data showed similar results under cool water immersion. Keatinge and McCance (15) assumed that an in­crease in peripheral venous pres­sure, as a result of cold exposition, led to a compression of the capaci-tative vascular system with an in­crease in central venous pressure. No evident data is available mea­suring central blood volume and central venous pressure under cool water immersion. Our data shows no difference in the release of ANF concerning 24 e C and 28 e C in comparison to thermoneutral 7 7 PMRvOL 3 NO 3 1991 baths. The increased atrial and ve­nous tonus within cool water might not allow a further central­ization of blood volume. For the immersion under hot con­ditions, however, our results dem­onstrate a stronger rise of ANF concentration in the plasma. Asanuma et al. (16) have also found relatively high values after baths of 10 minutes (40 eC). We have to consider several mecha­nisms concerning the ther-moregulative characteristics in hot baths. With rising core tem­perature in the bath we can espe­cially state an increase of heart rate, stroke volume, cardiac out­put and a reduction of peripheral resistance (17). The regulatory ad­justment of the circulation typi­cally leads to an increased skin perfusion with a reduction in the splanchnicus region at the same time. The mean sublingual temperature increased about 1 e C during baths of 40 minutes (39 eC). Higher core temperature might influence the ANF secretion, since a thermic de­pendence has been described in the isolated atrial preparation of the rat (18). At the same time the strong sympathicotonic reaction under hot water conditions leads to an increased release of cate­cholamines. This might be a con­tributing factor to higher release of ANF, because it is reported a re­sponse to the direct effect of adrenergic stimulation (19-23). Supposing that the atrial pressure is most important for the ANF stimulation, we have to consider that the haemodynamics corre­spond with an increase in atrial pressures. In contrast to this as­sumption, there is a reduction in atrial pressures if hot exposure takes place with air as the environ­mental medium (24). There are fewer results of atrial pressure measurements in warm baths. In warm baths (38 *C, 15 min) there were no alterations of central ve­nous pressures compared to ther­moneutral conditions (25). Other experiments, however, have shown a higher cardiac output (17). Obviously, the hydrostatic pressure prevents a peripheral ve­nous pooling and improves the ve­nous reflow. Possibly there is a mobilization of blood volume from the splanchnicus region, where the increase of vascular tonization also involves the venous vessels (24). Further discussions also stressed the importance of heart rate for the ANF release. Higher plasmatic ANF levels have been observed in patients suffering from paroxys­mal tachycardia (12-14), as well as with pacemaker induced tachy­cardia (26). Furthermore a rise of stimulation rate at the isolated atrial preparation led to an in­crease of ANF release (27). However, we have to ask for the in-terdependance of heart rate and atrial pressure. Patients with supraventricular tachycardia showed an increase of ANF plasma concentration as well as a rise of mean right atrial pressure (28, 29). There are similar effects with pacemaker tachycardia in a rabbit experiment (30). Corresponding with results in patients, an ANF ef­fect has not been achieved by a mere increase in heart rate (31). In a dog experiment an increase of heart rate during low atrial pres­sures did not correspond with an increased ANF release (32). In a recent study these authors tried to differentiate the influence of atrial pressure, atrial distension and heart rate. They were able to prove a higher correlation between ANF plasma concentration and the systolic atrial pressure in con­trast to mean atrial pressure. The highest concentration coefficient has been found for the heart rate and systolic atrial pressure prod­uct. It was concluded that within the determinants for ANF stimula­tion, the atrial distension is less than the increase in actual wall tension. In these experiments the influence of diastolic atrial filling is also evident. With an elevated diastolic atrial pressure, the atrial systolic pressure is potentiated, and only with high atrial pressure can heart rate play a major role in ANF stimulation. These findings might explain the relatively high ANF concentration we found under hot bath condi­tions. It can be hypothezised, that the hydrostatic pressure allows no more thermically dependent ve­nous pooling in the periphery, and thus guarantees a high cardiac preload. Thus the increased heart rate (74 min-1 to 103 min-1 in a 39 # C (bath) in combination with a more rapid rise in atrial systolic pressure could have a substantial effect on ANF secretion. References (1) De Bold AJ, Borenstein HB, Veress AT, Sonnenberg Η: A rapid and potent natri­uretic response to intravenous injection of atrial myocardial extracts in rats. Life Sei 1981;28:89-94. (2) Lang RE, Thoelken H, Ganten D, Luft FC. Ruskoaho Η, UngerTH: Atrial natriu­retic factor - a circulating hormone stimu­lated by volume loading. Nature Lond 1985;314:264-266. (3) Epstein M. Renal effects of head out water immersion in man. Implications for an understanding of volume homeostasis. Physiolopical Reviews 1978;58:529-581. (4) Anderson JV. Millar ND, O'Hara JP, Mackenzie J C . Corrall RJM, Bloom SR* Atrial natriuretic peptide: physiological re­lease associated with natriuresis during water immersion in man. Clinical Science 1986;71:319-322. (5) Epstein M, Loutzenhiser RD, Friedland Ε, Aceto RM, Camargo MJF, Atlas SA: Increases in circulating atrial natriuretic factor during immersion - induced central hypervolemia in normal humans. J of Hypertension 1986;4 (Suppl. 2):93-99. (6) GerbesAL. Arendt RM, Schnizer W. Silz S, Jüngst D, Zähringer J , Paumgartner G: Regulation of atrial natriuretic factor relea­se in man: Effect of water immersion. Klin Wochenschr 1986;64:666-667. (7) Gerbes AL, Arendt RM, Gerzer R, Schni­zer W, Jüngst D, Paumgartner G. Wernze H: Role of atrial natriuretic factor, cyclic GMP and the renin - aldosterone system in acute volume regulation of healthy hu­man subjects. European Journal of Clini­cal Investigation 1988;18:425-429. (8) Ogihara T, Shima J , Hara H, Tabuchi Y, Hashizume K. Nagano M. Katahira K. Kangawa K, Matsuo H, Kumahara Y: Signi­ficant increase in plasma immunoreactive atrial natriuretic peptide concentration during head-out water immersion. Life Sei 1986;38:2413-2418. (9) Pendergast DR. De Bold AJ, Pazik M. Hong SK: Effect of head-out immersion on plasma atrial natriuretic factor in man. Proc Soc Exp Biol Med 1987; 184:429-435. (10) ArendtRM. GerbesAL, Ritter D, Stangl E : Molecular weight heterogeneity of plas­ma - ANF in cardiovascular disease. Klin Wochenschr 1986;64 (Suppl. VI):97-102. (11) Gauer OH, Henry JP, Behn C: Hie regulation of extracellular fluid volume. Annu Rev Physiol 1970;32:547-595. PMRy° L 3 N o 3 1 9 9 1 (12) Schiffrin EL, Gutkowska J , Kuchel Ο, Cantin Μ, Genest J : Plasma concentration of atrial natriuretic factor in a patient with paroxysmal atrial tachycardia. Ν Engl J Med 1985:312:1196. (13) Tlkkanen I, Metsarinne K, Pyhrquist F: Atrial natriuretic peptide in paroxysmal supraventricular tachycardia. Lancet 1985;11:40-41. (14) Yamaji T, Ishibashi M, Nakaoka H, Imataka K, Amano M, Fujii J : Possible role for atrial natriuretic peptide in polyuria associated with paroxysmal atrial arrhyth­mias. Lancet 1985;i: 1211. (15) Keatinge WR McCance RA: Increase in venous and arterial pressures during sudden exposure to cold. The Lancet 1957;8:208-209. (16) Asanuma Y, Fujiya S, Ide H, Agishi Y: Augmentation of plasma atrial natriuretic peptide by hot water immersion in Normal man. J of Jap Ass Phys Med Bain and Clim 1988;51:199-206. (17) Weston CFM, O'Hare JP, Evans JM, Corral RJM: Haemodynamic changes in man during immersion in water at different temperatures. Clinical Science 1987;73:613-616. (18) Bilder GE, Schofield T L ; Blaine EH: Release of atrial natriuretic factor. Effects of repetitive stretch and temperature. Am J Physiol 1986;251 :F817-F821. ,·•'.:. (19) Currier MG, Newman WH: Evidence for -1 adrenergic receptor regulation of atriopeptin release from the isolated rat heart. Biochem Biophys Res Commun 1986;137:94-100. (20) Uhlinger DE, Weidmann W, Gnaedin-ger MP, Shaw S, Lang RE. Depressor effect and release of atrial natriuretic peptide during norepinephrine or angiotensin II infusion in man. J Clin Endocrinol Metab 1986;63:669-674. (21) Sanfield JA, Shenker Y, Grekin RJ , Rosen SG: Epinephrine increases plasma immunoreactive atrial natriuretic hormo­ne levels in humans. Am J Physiol 1987;252:E740-E745. (22) Schiebinger RJ , Baker MZ, Linden J : Effect of adrenergic and muscarinic choli­nergic agonists on atrial natriuretic pepti­de secretion by isolated rat atria. J Clin Invest 1987;80:1687-1691. (23) Donckier J , Michel L, Cpllard E» Bear* binschi A, Ketelsleger JM, Haryengt C, Buysschaert M: Parallel changes of atrial natriuretic factor and catecholamines du­ring surgery for pheochromocytoma. Am J of Med 1988;85:278-279. (24) Rowell LB: Cardiovascular adjust­ments to thermal stress. Handbook of Phy­siology. Section 2: The Cardiovascular System, Volume III. Bethesda, Maryland, 1983 (25) Franke Μ, Nietn Η, Kaufmann W: Ober die Wirkung balneotherapeutischer Maß­nahmen auf die Kreislaufhämodynamik unter besonderer Berücksichtigung der Nierenfunktion . Ζ angew Bäder? Klima-heilk 1966;13:415-449. (26) Crozier IG, Nicholls MG, Ikram H, Espiner EA; Yandle TG, Jans S: Atrial na­triuretic peptide in humans. Production and clearance by various tissues. Hyper­tension 1986;8 (SuppL II);II-11-II-15. (27) Schiebinger RJ , Linden J : Effect of atrial contraction frequency on atrial na­triuretic peptide secretion. Am J Physiol 1986a;251 :H 1095-H1099. (28) Nicklas JM, Dicarlo LA, Koller PT, Morady F, Diltz EA, Shenker Y, Grekin RJ: Plasma levels of immunoreactive atrial na­triuretic factor increases during supraven­tricular tachycardia. Am Heart J 1986;112:923-928. (29) Roy D, Paillard F. Cassidy D, Bourassa MG, Gutowska J , Genest J , Cantin M: Atrial natriuretic factor during atrial fibril­lation and supraventricular tachycardia. J Am Coll Cardiol 1987;9:509-514. (30) Rankin AJ, Wilson N, Ledsome JR: Effects of autonomic stimulation on plas­ma immunoreactive atrial natriuretic pep^ tide in the anesthetized rabbit. Can J Physiol Pharmacol 1987;65:532-537. (31) Haufe MC, Weil J , Nafeger K, Gerzer R, Bildlingmaier F, Theisen K: Acute in­crease in right atrial pressure by intracar­diac stimulation releases atrial natriuretic peptide. Eur Heart J 1987;8:277-281. (32) Christensen G, Ilebekk A, Aakeson J ; Fikil: The release mechanism for atrial na­triuretic factor during blood volume expan­sion and tachycardia in dogs. Acta Physiol Scand 1988; 134:263-270. Date Place Name Office (Information 1991 September 6-8 Copenhagen, Denmark 2nd Scientific meeting of the Scandinavian Medical Society of Paraplegia Centre for spinal cord injured, , Rigshospitalet, TH 2002, DK-2100 Copenhagen, Denmark October 23-27 Düsseldorf, Germany REHA '91 Exhibition and Congress - Rehabilitation Aids for Handicapped Persons NOWEA-Rehab'91, Postfach 32 02 03, Stockumer Kirchstraße 61, W-4000 Düsseldorf 30, Germany November 23 Vienna, Austria Annual meeting of the Austrian Society PMR Prim. Dr. Rathkolb, Hanusch-KH, Heinrich-Collinstraße 30,1140 Vienna, Austria December 8-12 Vienna, Austria Second Paneuropean Congress of Neurology Admin. Seer. Wiener Medizinische Akademie für Ärztliche Fortbildung und Forschung, Aiser Straße 4, A-1090 Wien/Vienna Austria 1992 September. 16-21 j . Bad Gottleuba Germany World Conference PMR Prof. Dr. Reinhold, . Kliniksanatorium, ErnstThälmann Straße 89, D-8302 Bad Gottleuba September 26-28 Dublin, Ireland Int. Physiotherapy Conference School of Physioth,, Trinty College, PO Box 814, James's Street, Dublin, Ireland 

A rapid and potent natri uretic response to intravenous injection of atrial myocardial extracts in rats.

Agishi Y: Augmentation of plasma atrial natriuretic peptide by hot water immersion in Normal man.

Annu Rev Physiol 1970;32:547-595.

Atlas SA: Increases in circulating atrial natriuretic factor during immersion - induced central hypervolemia in normal humans.

Atrial natriuretic factor during atrial fibril lation and supraventricular tachycardia.

Bloom SR* Atrial natriuretic peptide: physiological re lease associated with natriuresis during water immersion in man.

Corral RJM: Haemodynamic changes in man during immersion in water at different temperatures.

Depressor effect and release of atrial natriuretic peptide during norepinephrine or angiotensin II infusion in man.

E: Molecular weight heterogeneity of plas ma - ANF in cardiovascular disease.

Effect of adrenergic and muscarinic choli nergic agonists on atrial natriuretic pepti de secretion by isolated rat atria.

Effect of atrial contraction frequency on atrial na triuretic peptide secretion.

EH: Release of atrial natriuretic factor. Effects of repetitive stretch and temperature.

Fikil: The release mechanism for atrial na triuretic factor during blood volume expan sion and tachycardia in dogs. Acta Physiol Scand

Grekin RJ: Plasma levels of immunoreactive atrial na triuretic factor increases during supraven tricular tachycardia.

Keatinge WR McCance RA: Increase in venous and arterial pressures during sudden exposure to cold. The Lancet 1957;8:208-209.

LB: Cardiovascular adjust ments to thermal stress. Handbook of Phy siology. Section 2: The Cardiovascular System, Volume III.

Ledsome JR: Effects of autonomic stimulation on plas ma immunoreactive atrial natriuretic pep^ tide in the anesthetized rabbit.

Parallel changes of atrial natriuretic factor and catecholamines du ring surgery for pheochromocytoma.

Paumgartner G: Regulation of atrial natriuretic factor relea se in man: Effect of water immersion.

Plasma concentration of atrial natriuretic factor in a patient with paroxysmal atrial tachycardia.

Possible role for atrial natriuretic peptide in polyuria associated with paroxysmal atrial arrhyth mias. Lancet

Proc Soc Exp Biol Med

Pyhrquist F: Atrial natriuretic peptide in paroxysmal supraventricular tachycardia.

S: Atrial na triuretic peptide in humans. Production and clearance by various tissues. Hyper tension 1986;8

SG: Epinephrine increases plasma immunoreactive atrial natriuretic hormo ne levels in humans.

Signi ficant increase in plasma immunoreactive atrial natriuretic peptide concentration during head-out water immersion. Life Sei 1986;38:2413-2418. (9) Pendergast

Theisen K: Acute in crease in right atrial pressure by intracar diac stimulation releases atrial natriuretic peptide.

UngerTH: Atrial natriu retic factor - a circulating hormone stimu lated by volume loading. Nature Lond 1985;314:264-266. (3) Epstein M. Renal effects of head out water immersion in man. Implications for an understanding of volume homeostasis.

Wernze H: Role of atrial natriuretic factor, cyclic GMP and the renin - aldosterone system in acute volume regulation of healthy hu man subjects.

The effect of different water temperatures on the release of the atrial natriuretic factor (ANF) during "head out water immersion (HOI)"

http://epub.ub.uni-muenchen.de/5921/1/5921.pdf

The effect of different water temperatures on the release of the atrial natriuretic factor (ANF) during "head out water immersion (HOI)"

Abstract

Similar works

Full text

Available Versions

Open Access LMU