Atrial Natriuretic Peptide, Altitude and Acute Mountain Sickness

Milledge, J. S.; Beeley, J. M.; McArthur, Silvia Gatti; Morice, AH

doi:10.1042/cs0770509

Cited by 34 publications

(15 citation statements)

References 3 publications

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“…Whilst its underlying pathophysiology is not fully understood, increased levels of aldosterone and fluid retention have been found in persons suffering AMS (Hackett et al 1982;Milledge et al 1989), and RAS activation thus postulated to play an important contributory role (Bartsch et al 1988(Bartsch et al , 1991.…”

Section: Introductionmentioning

confidence: 98%

The effect of angiotensin-converting enzyme genotype on acute mountain sickness and summit success in trekkers attempting the summit of Mt. Kilimanjaro (5,895 m)

Kalson

Thompson²,

Davies

et al. 2008

Eur J Appl Physiol

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The I-allele rather than the D-allele of the human angiotensin converting enzyme (ACE) gene has been associated with high-altitude mountaineering success. We investigated whether the I-allele was associated with summit success, and also with AMS development, in altitude-naïve trekkers. Subjects ascended from 1,860 m to the summit over 4 days (n = 34, 'direct-profile') or 5 days (n = 82, 'slower-profile'). Proportionally more II direct-profile subjects were successful than ID or DD, although the difference was not significant (100% of II subjects, 52% ID and 43% DD, P = 0.09). There was no difference in success amongst subjects on the slower-profile (50% II, 45% ID and 58% DD, P = 0.54). There was a non-significant trend for increasing AMS scores in ID/DD subjects. Amongst tourist trekkers on Mt. Kilimanjaro the I-allele is not associated with summit success. No evidence is found to support an association between ACE genotype and AMS development.

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Section: Introductionmentioning

confidence: 98%

The effect of angiotensin-converting enzyme genotype on acute mountain sickness and summit success in trekkers attempting the summit of Mt. Kilimanjaro (5,895 m)

Kalson

Thompson²,

Davies

et al. 2008

Eur J Appl Physiol

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“…This might be explained by an increase in renal sympathetic activity induced by hypoxic stimulation of the peripheral chemoreceptors and/or by a reduction in renal perfusion pressure (Marshall, 1994). On the other hand, raised plasma levels of ANP have also been found in human subjects at high altitude (Milledge, Beeley, Me Arthur & Morice, 1989) in chronically hypoxic patients (Adnot et al 1989) and in rats that were kept in a hypoxic chamber for 1, 7 or 21 days (McKenzie, Tanka, Inagami, Misono & Klein, 1986; Winter, Meleagros, Pervez, Jamal, Krausz, Polak & Bloom, 1989). Increased secretion of ANP in chronic hypoxia might be explained by right atrial distension secondary to hyper‐ventilation, blood volume expansion or pulmonary hyper‐tension (e.g.…”

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confidence: 99%

The effects of chronic hypoxia on renal function in the rat

Neylon

Marshall²,

Johns

1997

The Journal of Physiology

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Studies were performed on rats that had been made chronically hypoxic (CH rats) in a normoxic chamber at 12% O2 for 3–5 weeks. Under Saffan anaesthesia, respiratory and cardiovascular variables, renal haemodynamics and renal function were recorded while the rats spontaneously breathed 12% O2 followed by a switch to air breathing for 20 min. Plasma renin activity was assessed by radioimmunoassay of angiotensin I. Plasma atrial natiruetic peptide (ANP) was indirectly assessed by measurement of cyclic GMP in urine. When breathing 12% O2, CH rats showed hyperventilation and raised haematocrit (52%) relative to normoxic (N) rats. But arterial pressure (ABP), renal blood flow (RBF), renal vascular conductance (RVC), mean right atrial pressure (mRAtP), urine flow, glomerular filtration rate (GFR) and absolute sodium excretion (UNaV) were comparable to those recorded in N rats breathing air. Urinary cGMP was 40% greater than in N rats, but plasma renin activity was not significantly greater in CH than in N rats. Air breathing in CH rats induced hypoventilation, a 12% increase in ABP, no change in mRAtP, RBF or GFR, but increases of 75 and 100% in urine flow and UNaV, respectively. Neither urinary cGMP nor plasma renin activity changed. Such increases in urine flow and UNaV were absent when renal perfusion pressure (RPP) was prevented from rising during air breathing by using an occluder on the dorsal aorta. We propose that by 3–5 weeks of chronic hypoxia renal function was normalized, principally because arterial O2 content was normalized by the increase in haematocrit and because ABP and renal haemodynamics were normalized: acute hypoxia in N rats produces a fall in ABP. We suggest that plasma ANP was raised by the actions of hypoxia or erythropoietin on the atrium, rather than by atrial distension, but suggest that ANP had little direct influence on renal function and tended to limit the influence of the renin–angotensin system. We further propose that the diuresis and natriuresis seen during air breathing were mediated by the increase in RPP; neither plasma ANP nor renin activity change in the immediate short term.

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“…A decreased renal excretory function has been observed at high altitude [28], but there is no general agreement as to how renal hemodynamics are affected. Short-term hypoxia decreased renal blood flow in anesthetized rats [29], unanesthetized rabbits [30,31], and anesthetized dog [32]; renal blood flow, however, remained unchanged in unanesthetized dogs [30] or even increased in man [33].…”

Section: Renal Blood Flowmentioning

confidence: 98%