Micropuncture study was performed in 21 mildly volume-expanded Munich-Wistar rats before and during partial aortic constriction to examine the effects of endogenous prostaglandins (PG) and angiotensin II (AII) on single nephron glomerular filtration rate (SNGFR) and absolute proximal reabsorption rate (APR). Animals received either vehicle (group 1), indomethacin (group 2), or indomethacin plus saralasin (group 3). Before aortic constriction, these inhibitors were without effect on values of SNGFR and APR. In group 1 rats, reduction in mean renal arterial perfusion pressure (RAP) to approximately 65 mm Hg resulted in marked and proportional declines in SNGFR and APR. With equivalent reduction in RAP in group 2 rats, however, SNGFR fell to a lesser extent and APR tended to increase slightly above preconstriction values. Indomethacin administration was therefore associated with disruption of glomerulotubular balance. In view of the roughly equivalent declines in afferent arteriolar resistance measured in groups 1 and 2, the magnitude of increase in efferent arteriolar resistance (R(E)) appeared to be of major importance in determining the observed presence or absence of glomerulotubular balance. Thus, the lesser fall in SNGFR in group 2 than in group 1 was a result of the higher value for glomerular capillary hydraulic pressure in group 2, a consequence of the higher value of R(E). The higher average value for APR during reduced RAP in group 2 than in group 1 is also attributable to this pronounced rise in R(E), the effect of which was to augment the net reabsorptive pressure both by favoring higher postglomerular oncotic pressure and lower downstream (peritubular capillary) hydraulic pressure. Since intrarenal release of AII is enhanced when RAP declines, and because AII is known to raise R(E) selectively, it is likely that endogenous AII brought about the marked increase in R(E) in group 2, which was readily demonstrable only in indomethacin-treated rats, presumably because endogenous PG synthesis was suppressed. In keeping with this conclusion, when the action of endogenous AII was inhibited by saralasin in group 3 rats, reduction in RAP failed to induce a rise in R(E), so that net filtration and reabsorption pressures again declined proportionally, as did SNGFR and APR. The present evidence therefore suggests that glomerulotubular balance is influenced to an important extent by the prevailing vasomotor tone of the efferent arteriole.

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Importance of efferent arteriolar vascular tone in regulation of proximal tubule fluid reabsorption and glomerulotubular balance in the rat.

Renal abnormality of essential hypertension

The sections in this article are:


1
Intrarenal Hemodynamic Control of Sodium Excretion
1.1
Effects of Peritubular Starling Forces on Sodium Excretion

1.2
Effects of Medullary Blood Flow on Sodium Excretion

1.3
Effects of Renal Perfusion Pressure on Sodium Excretion




2
Neural Control of Sodium Excretion
2.1
Sodium Intake and Body Fluid Volumes

2.2
Low-Pressure Baroreceptors

2.3
Renal Sympathetic Nerve Activity




3
Hormonal Control of Sodium Excretion
3.1
Renin–Angiotensin–Aldosterone System

3.2
Renal Prostaglandin System

3.3
Renal Kallikrein–Kinin System

3.4
Natriuretic Hormone

3.5
Atrial Natriuretic Peptide




4
Summary

Control of Sodium Excretion: An Integrative Approach

Dependency of proximal tubular fluid transport on the load of glomerular filtrate

The natriuresis and concomitant decline in absolute proximal reabsorption (APR) that occur in rats in response to saline loading are blunted markedly when renal perfusion pressure is reduced immediately before, but not after, the volume load. To ascertain the mechanism responsible for these differences between early clamp (EC) vs. late clamp (LC), intracapillary and interstitial determinants of peritubular capillary uptake of APR were measured in seven LC and seven EC Munich-Wistar rats before and after isotonic saline loading (80% body wt). With volume expansion in LC animals, we observed a marked decline in APR (averaging 11±1 nl/min), associated with large increases in urinary sodium excretion rate, which averaged 8±2 μeq/min. In EC, the changes in urinary sodium excretion rate (+1±0 μeq/min) and APR (−3±1 nl/min) with volume expansion were smaller in magnitude. Since peritubular capillary reabsorption coefficient and mean peritubular transcapillary hydraulic pressure difference did not change with saline loading in LC, the marked fall in APR was attributed primarily to a measured large decline in mean peritubular transcapillary oncotic pressure difference (). Despite an equivalent mean fall in with volume expansion in EC, near-constancy of APR was found to be associated with a simultaneous and equivalent decline in mean peritubular transcapillary hydraulic pressure difference (a consequence of decreased mean peritubular capillary hydraulic pressure), which effectively offset the fall in . These results demonstrate the importance of hydraulic pressure patterns of the peritubular capillaries in modulating APR and are consistent with the view that Starling forces across the postglomerular microcirculation play a fundamental role in determining APR.

/pdf/mechanism-of-inhibition-of-proximal-tubule-fluid-2egb5fkgrw.pdf

Mechanism of Inhibition of Proximal Tubule Fluid Reabsorption after Exposure of the Rat Kidney to the Physical Effects of Expansion of Extracellular Fluid Volume

Takao Wada

Papers

Effect of peritubular capillary perfusion rate on proximal sodium reabsorption