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The effects of chronic hypoxia on renal function in the rat
Author(s) -
Neylon Marie,
Marshall Janice M.,
Johns Edward J.
Publication year - 1997
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1997.243bo.x
Subject(s) - plasma renin activity , renal blood flow , medicine , renal function , endocrinology , chemistry , renin–angiotensin system , effective renal plasma flow , renal circulation , kidney , hyperventilation , ventilation (architecture) , atrial natriuretic peptide , mean arterial pressure , filtration fraction , urinary system , perfusion , blood pressure , heart rate , mechanical engineering , engineering
1 Studies were performed on rats that had been made chronically hypoxic (CH rats) in a normoxic chamber at 12% O 2 for 3–5 weeks. Under Saffan anaesthesia, respiratory and cardiovascular variables, renal haemodynamics and renal function were recorded while the rats spontaneously breathed 12% O 2 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. 2 When breathing 12% O 2 , 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 ( U Na V ) 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. 3 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 U Na V , respectively. Neither urinary cGMP nor plasma renin activity changed. Such increases in urine flow and U Na V were absent when renal perfusion pressure (RPP) was prevented from rising during air breathing by using an occluder on the dorsal aorta. 4 We propose that by 3–5 weeks of chronic hypoxia renal function was normalized, principally because arterial O 2 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.