title: Functional response to graded increases in renal nerve activity during hypoxia in conscious rabbits.
abstract: Changes in renal sympathetic nerve activity (SNA) are postulated to influence renal function in selective ways, such that different levels of activation produce particular renal responses, initially in renin release, then sodium excretion, with changes in renal hemodynamics occurring only with much greater stimulus intensities. The aim of this study was to determine the renal hemodynamic and excretory responses to graded physiological increases in renal SNA induced by breathing different hypoxic gas mixtures. Experiments were performed in seven conscious rabbits subjected to four gas mixtures (14% O2, 10% O2, 10% O2 + 3% CO2, and 10% O2 + 5% CO2) and instrumented for recording of renal nerve activity. After a 30-min control period, rabbits were subjected to one of the four gas mixtures for 30 min, and then room air was resumed for a further 30 min. The four gas mixtures increased renal SNA by 14, 38, 49, and 165% respectively, but arterial pressure (thus renal perfusion pressure) was not altered by any of the gas mixtures. The greatest level of sympathetic activation produced significant falls in glomerular filtration rate (GFR), renal blood flow, sodium and fluid excretion, and significant increases in plasma renin activity. These returned to levels not significantly different from control conditions in the 30-min period after the gas mixture. When the changes to the various gas mixtures were analyzed within each rabbit, a significant linear relationship was found with all variables to the increase in SNA. Renal denervation in a separate group of seven rabbits completely abolished all of the above responses to the different gas mixtures. Thus graded activation of renal nerves induced by changes in inspired gas mixtures resulted in graded decreases in renal blood flow, GFR, and sodium excretion and graded increases in renin activity, with the changes occurring across a similar range of nerve activities; there was no evidence for a selective change in any renal variable.
authors.affiliation: Baker Medical Research Institute, Prahran, Victoria, Australia.
authors.forename: S C
authors.initials: SC
authors.lastname: Malpas
authors.forename: A
authors.initials: A
authors.lastname: Shweta
authors.forename: W P
authors.initials: WP
authors.lastname: Anderson
authors.forename: G A
authors.initials: GA
authors.lastname: Head
mesh_terms: D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology; D003714:Denervation; D004231:Diuresis / Q000187:drug effects; D004338:Drug Combinations; D005919:Glomerular Filtration Rate; D006439:Hemodynamics / Q000187:drug effects; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects / Q000294:innervation* / Q000503:physiopathology; D009318:Natriuresis; D010100:Oxygen / Q000494:pharmacology; D011817:Rabbits; D012079:Renal Circulation / Q000187:drug effects; D012083:Renin / Q000097:blood; D013564:Sympathetic Nervous System / Q000503:physiopathology*
chemical_list: D004338:Drug Combinations; D002245:Carbon Dioxide; D012083:Renin; D010100:Oxygen