Regulation of the Extracellular Fluid Volume and Renal Function

2010 ◽  
pp. 239-267 ◽  
Author(s):  
Jens H. Henriksen
1979 ◽  
Vol 56 (6) ◽  
pp. 547-553 ◽  
Author(s):  
H. J. Kramer ◽  
T. Moch ◽  
L. Von Sicherer ◽  
R. Düsing

1. Aprotinin, a potent kallikrein inhibitor, was given to conscious rats with and without expansion of the extracellular fluid volume with isotonic saline. 2. In noa-expanded rats aprotinin had no effect on arterial pressure, glomerular filtration rate (GFR), hippuran clearance, urinary flow rate, absolute sodium and potassium excretion or free-water clearance. 3. In volume-expanded rats aprotinin significantly reduced GFR, hippuran clearance, urine volume (V) UNaV, UKV and Cwater/GFR without effect on systemic arterial pressure. 4. Urinary immunoreactive prostaglandin E2 excretion significantly increased during the expansion phase but returned to below the control range during stable extracellular fluid volume expansion. 5. Aprotinin significantly suppressed urinary immunoreactive prostaglandin E2 excretion in non-expanded rats and in volume-expanded rats during the expansion phase, but not during stable expansion. 6. The results suggest that the kallikrein-kinin system may contribute to changes in renal function during extracellular volume expansion. This action may not necessarily be associated with changes in renal prostaglandin E2 activity.


1999 ◽  
Vol 276 (6) ◽  
pp. R1551-R1561 ◽  
Author(s):  
Branko Braam

If, only 20 years ago, anyone had postulated that the absence of nitric oxide gas (NO) would lead to severe hypertension and destruction of the vascular bed of the kidney within weeks, it is not unlikely that smiles of pity would have appeared on the faces of fellow researchers. By now, this has become common knowledge, and hundreds of reports have appeared on the regulation of vascular and renal function by nitric oxide. The amount of information complicates the design of a concept on how NO participates in control of extracellular fluid volume (ECFV) by the kidney. This review analyzes the function of endothelial and macula densa NO synthase (NOS) in the regulation of renal function. From this analysis, endothelial NOS (eNOS)-derived NO is considered a modulator of vascular responses and of renal autoregulation in particular. Increases in renal perfusion pressure and sodium loading will increase eNOS activity, resulting in vasodilatation and depression of tubuloglomerular feedback system responsiveness. Endothelium-derived NO seems important to buffer minute-to-minute variations in perfusion pressure and rapid changes in ANG II activity. In contrast, macula densa NOS is proposed to drive adaptations to long-term changes in distal delivery and is considered a mediator of renin formation. Increases in perfusion pressure and distal delivery will depress the activity and expression of the enzyme that coincides with, and possibly mediates, diminished renin activity. Together, the opposite responses of eNOS and macula densa NOS-derived NO to changes in ECFV lead to an appropriate response to restore sodium balance. The concept that the two enzymes with different localizations in the kidney and in the cell are producing the same product, displaying contrasting responses to the same stimulus but nevertheless exhibiting an integrated response to perturbation of the most important regulated variable by the kidney, i.e., the ECFV, may be applicable to other tissues.


Urinary tract morphology The kidney 474 The ureters 478 The bladder 480 Histology of the urinary tract 482 Renal function Glomerular filtration 486 Tubular transport 490 Dilute and concentrated urines 494 Regulation of tubule function 496 Diuretics 498 Regulation of body fluids Regulation of extracellular fluid volume and osmolarity ...


1958 ◽  
Vol 192 (2) ◽  
pp. 401-404 ◽  
Author(s):  
Sydney M. Friedman ◽  
Harald F Scherrer ◽  
Miyoshi Nakashima ◽  
Constance L. Friedman

Using inulin as indicator of the extracellular volume, the distribution of sodium, potassium and water was studied in rats with diabetes insipidus produced by interrruption of the supraoptico-hypophyseal tract. A well defined increase in the extracellular fluid volume associated with normal plasma sodium and reduced plasma potassium concentration was uniformly present in the rats with diabetes insipidus. These changes occurred in nephrectomized animals and were thus independent of renal function, but were in some degree referable to an increase in adrenal function since they could be partially reversed by adrenal ablation.


1978 ◽  
Vol 28 ◽  
pp. 179
Author(s):  
Toshiaki Kadokawa ◽  
Kanno Hosoki ◽  
Kunihiko Takeyama ◽  
Hisao Minato ◽  
Masanao Shimizu

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