Renal Function, Urinary Flow Rates and Diuresis Renography

Author(s):  
S. C. W. Brown ◽  
S. M. Upsdell ◽  
C. D. Betts ◽  
P. H. O�Reilly
2000 ◽  
Vol 278 (1) ◽  
pp. R28-R33 ◽  
Author(s):  
John M. Stulak ◽  
Luis A. Juncos ◽  
John A. Haas ◽  
J. Carlos Romero

Cross-linked hemoglobin (XL-Hb) infused into dogs increases mean arterial pressure (MAP) but decreases blood flow to the renal (RBF), mesenteric (MBF), and iliac (IBF) circulations. These actions differ markedly from dextran infusion (which increases RBF, MBF, and IBF without altering MAP) and may be due to scavenging of nitric oxide by XL-Hb. However, because the hormonal milieu regulating regional circulation is altered during hemorrhage (when XL-Hb may be used), we studied whether systemic hemodynamics, RBF, MBF, IBF, and renal excretory function in hemorrhaged dogs was altered when resuscitated with XL-Hb compared with dextran ( n = 6 each). Hemorrhage decreased MAP by 25% due to a 75% decline in cardiac output. RBF, MBF, and IBF all fell by 33, 64, and 72%, respectively ( P < 0.05 each). There was also a fall in glomerular filtration rate (GFR), urinary flow, and sodium excretion ( P < 0.05 each). After resuscitation, MAP, cardiac output, RBF, MBF, IBF, and GFR all recovered to basal values with either XL-Hb or dextran. Urinary flow and sodium excretion increased to above basal levels with dextran (both by 3.5-fold; P < 0.05) or XL-Hb (by 7.5- and 10-fold, respectively; P < 0.05). We conclude that resuscitation with XL-Hb after hemorrhage not only increases MAP, but also restores RBF, MBF, IBF, GFR, and urinary sodium and volume excretion analogously to dextran. The results contrast with those in normal dogs and suggest that nitric oxide inhibition does not impair hemodynamic and renal function recovery during hemorrhage.


The Prostate ◽  
1998 ◽  
Vol 34 (2) ◽  
pp. 121-128 ◽  
Author(s):  
Alessandro Sciarra ◽  
Giuseppe D'Eramo ◽  
Paolo Casale ◽  
Andrea Loreto ◽  
Maurizio Buscarini ◽  
...  

Urology ◽  
1997 ◽  
Vol 49 (3) ◽  
pp. 476-480 ◽  
Author(s):  
Herbert Lepor ◽  
Alan Nieder ◽  
Jean Feser ◽  
Caroline O'Connell ◽  
Christopher Dixon
Keyword(s):  

1983 ◽  
pp. 523-527 ◽  
Author(s):  
Terry N. Layton ◽  
George W. Drach
Keyword(s):  

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.


1983 ◽  
Vol 105 (1) ◽  
pp. 351-362 ◽  
Author(s):  
A. J. MCVICAR ◽  
J. C. RANKIN

1. Improved estimates of urine flow rates of lampreys in various salinities were obtained by the collection of urine for periods of up to 48 h from minimally-stressed, unanaesthetized fish, following catheterization of the urinogenital papilla. 2. The mean urine flow rate of freshwater lampreys was 200.7 ±14.3 ml kg−1 day−1. 3. Urine flow in freshwater lampreys was correlated with spontaneous changes in gill ventilation rate. MS222 anaesthesia reduced both ventilation and urine flow rates, but pronounced effects were only observed at concentrations greater than those needed to induce light anaesthesia (50–55 mg 1−1). Urine flow rate in unanaesthetized fish was extremely sensitive to rapid (6°Ch−1) changes in temperature and Q10 (6–16°C) was approximately 5. 4. Urine flow rate decreased rapidly as the osmotic difference between the body fluids and environment approached zero, and the rate of flow in 30% seawater lampreys was only 7.6% that of freshwater fish. 5. There was no evidence for an effect of environmental calcium concentration on branchial osmotic permeability. 6. Extensive tubular reabsorption of ions occurred in freshwater lampreys. The total daily excretion rate of sodium ions generally decreased in salinities hyperosmotic to the plasma, indicating enhanced reabsorption, but secretion of magnesium and sulphate ions was greatly increased. Urine osmolarity was significantly increased in lampreys in hyperosmotic salinities. 7. Present data compare favourably with data obtained previously from anaesthetized animals, indicating that renal function in lampreys is not significantly impaired by light MS222 anaesthesia.


1986 ◽  
Vol 250 (2) ◽  
pp. F294-F301 ◽  
Author(s):  
J. E. Robillard ◽  
K. T. Nakamura ◽  
G. F. DiBona

The role of renal nerves in mediating renal hemodynamics and renal function during normal physiological conditions and following moderate hypoxemia was studied in chronically catheterized fetal lambs (125-141 days of gestation) following unilateral renal denervation. Base-line values for renal blood flow (RBF), renal vascular resistance (RVR), glomerular filtration rate (GFR), urinary flow rate (UFR), urinary electrolyte (Na+, K+, and Cl-) excretion rate, and urine osmolality (Uosm) were similar in both intact and denervated kidneys. Hypoxemia was associated with a significant rise in mean arterial blood pressure and a significant decrease in heart rate. Hypoxemia produced a similar decrease in GFR and similar increases in urinary Na+ and Cl- excretion rates in both intact and denervated kidneys. However, the effect of hypoxemia on renal hemodynamics differed between intact and denervated kidneys. Hypoxemia produced a continuous and progressive decrease in RBF and increase in RVR in the intact kidney. On the other hand, renal denervation was associated with an early renal vasodilation and attenuated the reduction in RBF and the rise in RVR during hypoxemia; this early renal vasodilation was blunted following prostaglandin synthesis inhibition. Taken together, these results suggest that fetal renal denervation is not associated with significant changes in renal hemodynamics or renal function during normal physiological conditions but that renal denervation partially inhibited the renal vasoconstriction associated with fetal hypoxemia. Finally, it was found that endogenous prostaglandins counteract the renal vasoconstriction associated with fetal hypoxemia.


2011 ◽  
Vol 30 (8) ◽  
pp. 1571-1575 ◽  
Author(s):  
Luca Cindolo ◽  
Cosimo De Nunzio ◽  
Petros Sountoulides ◽  
Athanasios Bantis ◽  
Andrea Tubaro ◽  
...  
Keyword(s):  

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