Renal and neurohormonal responses to increasing levels of lower body negative pressure in men

Background. The stimulation of efferent renal sympathetic nerve activity in duces sequential changes in renin secretion, sodium excretion, and renal he modynamics that are proportional to the magnitude of the stimulation of sym pathetic nerves. This study in men investigated the sequence of the changes in proximal and distal renal sodium handling, renal and systemic hemodynam ics, as well as the hormonal profile occurring during a sustained activatio n of the sympathetic nervous system induced by various levels of lower body negative pressure (LBNP). Methods. Ten healthy subjects were submitted to three levels of LBNP rangin g between 0 and -22.5 mm Hg for one hour according to a triple crossover de sign, with a minimum of five days between each level of LBNP. Systemic and renal hemodynamics, renal water and sodium handling (using the endogenous l ithium clearance technique), and the neurohormonal profile were measured be fore, during, and after LBNP. Results. LBNP (0 to -22.5 mm Hg) induced an important hormonal response cha racterized by a significant stimulation of the sympathetic nervous system a nd gradual activations of the vasopressin and the renin-angiotensin systems . LBNP also gradually reduced water excretion and increased urinary osmolal ity. A significant decrease in sodium excretion was apparent only at -22.5 mm Hg. It was independent of any change in the glomerular filtration rate a nd was mediated essentially by an increased sodium reabsorption in the prox imal tubule (a significant decrease in lithium clearance, P < 0.05). No sig nificant change in renal hemodynamics was found at the tested levels of LBN P. As observed experimentally, there appeared to be a clear sequence of res ponses to LBNP, the neurohormonal response occurring before the changes in water and sodium excretion, these latter preceding any change in renal hemo dynamics. Conclusions. These data show that the renal sodium retention developing dur ing LBNP, and thus sympathetic nervous stimulation, is due mainly to an inc rease in sodium reabsorption by the proximal segments of the nephron. Our r esults in humans also confirm that, depending on its magnitude, LBNP leads to a step-by-step activation of neurohormonal, renal tubular, and renal hem odynamic responses.