Possible role of juxtaglomerular apparatus in low cardiac output syndrome and multiple organ failure: modulation by high sodium load

Sympathetic overdrive in acute low cardiac output syndrome, diverts blood: from cutaneous and visceral circulation centripetally. Microcirculation in general, and renal circulation in particular, deteriorates during these cir culatory adjustments leading to multi-organ failure (MOF). Decreased affere nt glomerular arteriolar blood flow, increased renal sympathetic nerve disc harge and a resultant decreased sodium chloride delivery around macula dens a stimulates the Juxta-glomerular apparatus (JGA) and triggers renin-angiot ensin-aldosterone mechanism. This, along with increased ADH production resu lts in a state of vasoconstriction, increased after-load, and continued-flu id retention, further compromising the visceral microcirculation. initially the fluid retention under the effect of aldosterone and ADH is iso-osmotic , but later under inappropriate ADH action more water than salt is retained , as evidenced by the presence of hyponatraemia and 'water-logging' in the endstage of this condition. The author hypothesizes that: although physiological, the persistent stimul ation of the JGA during the low cardiac output state plays an important rol e in perpetuating a negative cardiovascular vicious cycle and further aggra vating it into MOF. Furthermore, by infusing hypertonic saline and hence in creasing the sodium chloride delivery to the distal tubules and the macula densa, the JGA could be inhibited. This strategy should work like angiotens in-converting-enzyme-inhibitor drugs in chronic cardiac failure, except by acting at the root cause and inhibiting Renin production at its source. It should further help by stimulating atrial natriuretic peptide secretion. (C ) 2001 Harcourt Publishers Ltd.