Hydrostatic pressure in the rat kidney

A B S T R A C T The hemodynamics of the rat kidney were studied during reduction ofrenal arterial pressure to 35-40 mm Hg (H), and after volume expansion at that pressure with 0.9% NaCl (IS), 1.7% NaCl (HS), 5% mannitol in 0.9% NaCl (MS), 5% mannitol in water (MW), or 50 mM mannitol + 125 mM NaCl. During H, left renal blood flow (RBF) was 0.8±0.1 ml/min. Expansion with IS did not alter RBF, but expansion with HS, MS, MW, and 50 + 125 mM NaCl elevated RBF to 200-250% of hypoperfusion values. Glomerular capillary pressure rose significantly from 15.7±0.7 mm Hg during H to 22.3+1.1, 24.4±0.7, and 26.6±0.7 mm Hg following expansion with HS, MS, or MW, respectively. Efferent arteriolar pressure also rose significantly to 6.9+0.5, 9.7±0.8, and 9.5±0.9 mm Hg, respectively. Preglomerular resistance fell to 18-24% of H values, and postglomerular resistance fell to 58-74% of H values after expansion with HS, MS, or MW. Glomerular filtration (GFR) could not be detected during H or after IS expansion. HS and mannitol-containing solutions restored GFR to 0.10±0.02-0.15±0.02 ml/min, and single nephron glomerular filtration to 6-12 nl/min. Papaverine, acetylcholine, and kinins had no effect on RBF or GFR at a perfusion pressure of 35-40 mm Hg. We conclude that mannitol and HS have the capacity to augment RBF during hypoperfusion by reducing arteriolar resistance. The mechanism of the rise in RBF is uncertain; it may be due to changes in effective osmolality of the extracellular fluid or to a direct action of mannitol on vascular smooth muscle. Other potent vasodilators were ineffective during hypoperfusion.

Section: Methodsmentioning

confidence: 99%

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Johnston¹,

Bernard²,

Donohoe³

et al. 1979

“…One of the mechanisms underlying the first of these two postulates might be that put forward by Leyssac (33) who assumed that a decrease in tubular reabsorption lowers the effective filtration pressure (EFP) and, therefore, the filtration rate. Although the validity of the experiments which support this theory has been questioned (34,35), one of the essential features of such a mechanism, namely the ability of the proximal tubular wall to withstand a moderate transmural hydrostatic pressure difference, has been demonstrated recently (36,37). Moreover, two studies (21,37) have revealed an even greater hydrostatic pressure gradient across the proximal tubular wall of young animals.…”

Section: Methodsmentioning

confidence: 99%

“…Although the validity of the experiments which support this theory has been questioned (34,35), one of the essential features of such a mechanism, namely the ability of the proximal tubular wall to withstand a moderate transmural hydrostatic pressure difference, has been demonstrated recently (36,37). Moreover, two studies (21,37) have revealed an even greater hydrostatic pressure gradient across the proximal tubular wall of young animals. It can also be considered that a low proximal tubular reabsorption will result in an increased delivery of filtrate to the macula densa, which, by a feedback mechanism, will result in a decrease in glomerular filtration rate (38)(39)(40).…”

Section: Methodsmentioning

confidence: 99%

Functional and Morphologic Maturation of the Superficial Nephrons RELATIONSHIP TO TOTAL KIDNEY FUNCTION

Spitzer¹,

Brandis²

1974

141

A B S T R A C T The functional and morphologic pattern of superficial nephron development was studied in guinea pigs ranging in age between 2 h and 38 days. Concomitent measurements of total kidney function and glomerular counts were also performed.Superficial nephron glomerular filtration rate was found to increase from 0.92 to 19.32 nl/min. The filtration rate of the entire kidney rose from 0.19 to 1.31 ml/ min. During the first 15 days of life the average rate of increase in glomerular filtration rate per nephron (0.48 nl/min-day), obtained by dividing the increase in total kidney glomerular filtration rate by glomerular number, was more than twice the observed rate of increase in the superficial nephrons (0.21 nl/min-day). During the remainder of the first month, the increase in superficial nephron glomerular filtration rate (0.97 nl/min-day) was greater than the average increase for all nephrons (0.71 nl/min-day). Thus, the initial increase in total kidney glomerular filtration rate was primarily a consequence of the activity of the deep nephrons, whereas during the ensuing period the superficial nephrons appeared to be the sole contributors to the change in total kidney glomerular filtration rate.The increase in superficial nephron glomerular filtration rate was found to correlate closely with the increase in proximal tubular length. Functional glomerulotubular balance was maintained throughout the entire period of renal maturation.

“…The whole sample was then discharged into counting fluid. The following calculations were made: SNGFR = F/P inulin X tubular flow rate in nl/min Percent reabsorption to the late proximal convolution ( F/P inulin) X Absolute reabsorption = fractional reabsorption X SNGFR nl/min In the second group (15 AICN, five anti-GBM, and seven control rats) the kidney was bathed with isotonic saline heated to 36±10C in order to allow the use of an electronic servo-nulling device for measurement of hydrostatic pressure as previously described (28). Sharpened, siliconized glass pipettes, external tip diameter 3-5 Aum, filled with 2 M NaCl were used to measure hydrostatic pressure in proximal tubules during free flow, in the large efferent arterioles or stars, in intermediate vessels, which are large diameter straight vessels and which often arise from stars, and in the larger peritubular capillaries.…”

Section: Methodsmentioning

confidence: 99%

Pathophysiology of Experimental Glomerulonephritis in Rats

Allison¹,

Wilson²,

Gottschalk³

1974

158

A B S T R A C T Micropuncture, clearance, immunofluorescence and light microscopy techniques were used to study kidney structure and single nephron function in rats with autologous immune complex nephritis (AICN), a membranous glomerulonephritis developing over 5 to 20 mo, in the more acute and proliferative glomerular basement membrane (GBM) nephritis and in controls. Both models are known to have clinical counterparts in human disease. Kidney functional abnormalities correlated with the degree of architectural derangement. In both AICN and anti-GBM nephritis filtration fraction fell in direct proportion to the fall in glomerular filtration rate (GFR), renal plasma flow being unchanged. Fractional electrolyte excretion increased as the GFR fell. Despite marked heterogeneity of single nephron filtration rate (SNGFR) (AICN, 5-93 nl/min; anti-GBM, 0-50 nl/min) and of proximal tubular hydrostatic pressure (4-48 mm Hg), each nephron showed almost complete glomerulotubular balance, absolute reabsorption to the late proximal convolution varying directly with filtration rate. In addition SNGFR could be related both to proximal intratubular hydrostatic pressure and to calculated glomerular capillary pressure (Pg), being lowest in those nephrons with the highest intratubular pressure. Nephrons with very high filtration rates did not apparently reach filtration equilibrium. Mean SNGFR was significantly lower in the anti-GBM group, while calculated Pg was the same in both. This probably reflects the acute and diffuse involvement of the anti-GBM lesion with different filtration characteristics from Dr.