Relation between sodium intake, renal function, and the regulation of arterial pressure.

Abstract

The long-term regulation of arterial pressure requires the maintenance of a balance between sodium and water intake and sodium and water excretion. Normal salt and water balance leads to stable body fluid volumes and the maintenance of normal renal function is critical to establishing extracellular fluid volume homeostasis. This review focuses on the role of the kidney in the long-term control of salt and water balance with particular emphasis on the relations between sodium intake, the renin-angiotensin-aldosterone system, renal sympathetic nerve activity, and the regulation of arterial pressure via renal sodium and water excretion. T he regulation of the extracellular fluid volume encompasses the continuous, ongoing maintenance of normal sodium and water balance as a relation between sodium intake and excretion. As humans, we exist as intermittent sodium and water consumers, leaving the bulk of the task of regulating our constant expansion of extracellular fluid volumes to the renal excretory processes. There are many factors that influence renal sodium excretion and thereby participate in this regulatory process. These factors can be subdivided into extrinsic and intrinsic mechanisms. Extrinsic mechanisms include the production of angiotensin II (Ang II) and aldosterone, the release of atrial natriuretic factor, and the alterations of renal sympathetic outflow; some intrinsic mechanisms are the regulation of glomerular filtration rate, renal hemodynamics, intrarenal physical forces controlling tubular reabsorp- Supported by an American Heart Association Established Investigator Award, by an American Heart Association Grant-inAid, and by National Heart, Lung, and Blood Institute grants HL-40137 and HL-29587.Address for correspondence: Jeffrey L. Osborn, PhD, Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226. tion, and intrarenal hormonal systems such as kinins, Ang n, and prostaglandins. Renal Function and Arterial PressureA close correlation between normal kidney function and blood pressure control has been demonstrated in several experimental forms of hypertension including the spontaneously hypertensive rat (SHR) 1 and the Dahl salt-sensitive (DS) rat.2 The spontaneously hypertensive strain of rats develops elevated arterial pressure spontaneously with age, and in some strains this hypertension is exacerbated with elevated sodium chloride intake. Kawabe et al 3 have shown that in this strain, replacement at an early age of the SHR kidneys by transplantation with kidneys from age-matched normotensive control rats results in a substantial diminution of the blood pressure. This same response has been shown in other genetic models of hypertension including the Milan hypertensive strain 4 and the DS rat. 5 Thus, a direct correlation has been documented between renal function and arterial pressure in several genetic models of hypertension, and in some strains a critical interaction exists between sodium intake and the magnitude of the hypertension.The complex relations between the natriu...

Renal nerves affect rate of achieving sodium balance in spontaneously hypertensive rats.

“…These renal responses to chronic changes in sodium intake are not different from those in Sprague-Dawley rats as previously observed in our laboratory 10 ; however, they are different from the antinatriuretic responses of conscious dogs. 15 Thus, any elevation of sympathetic tone that may exist in the SHR does not appear to be manifested as an alteration in the regulation of daily sodium balance but rather as a requirement to sustain MAP at a level consistent with other controllers of urinary sodium excretion.…”

Effects of fluorotelomer alcohol 8:2 FTOH on steroidogenesis in H295R cells: Targeting the cAMP signalling cascade

“…In addition, exposure to 8:2 FTOH in H295R cells also caused significant decreases in deoxycorticosterone, corticosterone and cortisol production. These hormones are associated with a variety of physiological processes including metabolism, stress responses, immune responses, vasoconstriction, growth, development, salt and water homeostasis and vascular tone (Mommsen et al, 1999;Osborn, 1991). Studies have shown that decreased production of these hormones may impair normal physiological processes and cause pathologic effects in vivo (Peter et al, 1999;Ueshiba et al, 2002).…”

Salt sensitivity in hypertension. Renal and cardiovascular implications.

“…59 Stimulation of renal sympathetic outflow may alter renal function and the normal relation between arterial pressure and natriuresis and diuresis. 60 Thus, an increase in renal sympathetic nerve activity could shift the pressure-natriuresis relation toward higher pressure and be responsible for the sodium retention. 61 -64 More recently, we observed that the blood levels of norepinephrine achieved during the infusion of fixed amounts of this hormone were lower in salt-sensitive than salt-resistant patients, suggesting substantial differences in norepinephrine metabolism between these two groups.…”