Renal interstitial hydrostatic pressure and sodium excretion in hypertension and pregnancy.
The kidney plays an important role in the long-term regulation of blood pressure and extracellular fluid volume through the regulation of sodium and water excretion. Increases in renal perfusion pressure (RPP) cause a potent natriuretic stimulus, referred to as 'pressure natriuresis', which is an important mechanism in the regulation of extracellular fluid volume and blood pressure. In normotensive animals, increases in RPP are transmitted to the renal interstitium and result in increases in renal interstitial hydrostatic pressure (RIHP), as well as in sodium and water excretion. However, pressure natriuresis is significantly attenuated in hypertensive and pregnant normotensive rats. Furthermore, this response is associated with an attenuated increase in RIHP with increases in RPP, suggesting that the renal interstitial compliance is greater in hypertension and during pregnancy than in normotensive non-pregnant states. In the absence of other mechanisms, this attenuated pressure natriuretic response can lead to volume retention. However, volume expansion also increases RIHP and sodium excretion. It is proposed that a compensatory increase in the natriuretic sensitivity to increases in RIHP counterbalances the volume retention that results from the attenuated pressure natriuresis in hypertensive rats, and thus may play an important role in maintaining normal plasma volume in these animals. Likewise, it is also proposed that the attenuated relationship between blood pressure, RIHP and sodium excretion that is observed during normal pregnancy is due to an increase in the compliance of the renal interstitium and leads to a reduction in sodium excretion and the gradual gestational volume expansion. During pregnancy, RIHP does not increase immediately due to the large renal interstitial compliance and therefore the increased sensitivity of the natriuretic response to increases in RIHP does not occur, and gradual volume expansion continues during normal pregnancy. However, the increased sensitivity of the natriuretic response to increases in RIHP takes effect only after the necessary volume is retained for a normal pregnancy. Below this requisite volume expansion, the increase in RIHP is not sufficient to activate the exaggerated natriuretic sensitivity to increases in RIHP. Failure of these adaptive mechanisms during pregnancy can lead to disturbances in the regulation of plasma volume which, in turn, can affect amniotic fluid volume and fetal growth and may result in premature labour and intrauterine growth restriction, as well as pre-eclampsia.
Department of Physiological Sciences, Eastern Virginia Medical School, PO Box 1980, 700 Olney Road, Norfolk, VA 23501-1980, USA. khraibaa@evms.edu
Ali A
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Khraibi
D000818:Animals; D001794:Blood Pressure; D001834:Body Water / Q000378:metabolism; D005260:Female; D006801:Humans; D006874:Hydrostatic Pressure; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000502:physiology*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D051381:Rats; D012964:Sodium / Q000378:metabolism*
D012964:Sodium