Effect of Imidazole on the Dynamics of Glomerular Ultrafiltration in the Rat

1979 ◽  
Vol 2 (5) ◽  
pp. 278-288 ◽  
Author(s):  
Christine Baylis
Keyword(s):  
Glomerular Ultrafiltration

Filtration by superficial and deep glomeruli of normovolemic and volume-depleted rats

1986 ◽  
Vol 250 (1) ◽  
pp. F86-F91
Author(s):  
R. V. Pinnick ◽  
V. J. Savin
Keyword(s):  
Basement Membrane ◽  
Maximum Rate ◽  
Rate Of Change ◽  
The Other ◽  
Membrane Area ◽  
Morphometric Analyses ◽  
Three Samples ◽  
Glomerular Size ◽  
Glomerular Ultrafiltration

We measured glomerular ultrafiltration coefficient (Kf) of isolated superficial (S) and deep (D) glomeruli of normovolemic and volume-depleted rats. Filtration was induced in vitro, and Kf was calculated from the maximum rate of change in glomerular size. Basement membrane area (A) for each glomerulus was estimated from morphometric analyses, and glomerular capillary hydraulic conductivity (Lp) was calculated by the formula Lp = Kf/A. Kf of S and D glomeruli of normovolemic rats were 2.98 +/- 0.98 and 4.25 +/- 0.07 nl . min-1 . mmHg-1, respectively. In hypovolemic rats, Kf of S glomeruli fell by approximately 50% to 1.52 +/- 0.14 nl . min-1 . mmHg-1 (P less than 0.001), whereas Kf of D glomeruli remained unchanged at 4.28 +/- 0.10 nl . min-1 . mmHg-1. Lp, calculated using the peripheral capillary area, averaged 1.98 +/- 0.09 and 1.98 +/- 0.06 microliter . min-1 . mmHg-1 . cm-2 in S and D glomeruli of normovolemic rats and 1.89 +/- 0.11 microliter . min-1 . mmHg-1 . cm-2 in D glomeruli of hypovolemic rats. Lp of S glomeruli of volume-depleted rats (0.90 +/- 0.03 microliter . min-1 . mmHg-1 . cm-2) was lower than in any of the other three samples. Mild hypovolemia causes the Kf of S glomeruli to decline, whereas Kf of D glomeruli remains constant. The decrease in Kf occurs without an alteration in capillary area and is most likely due to a decrease in Lp.

A model of glomerular ultrafiltration in the rat

1972 ◽  
Vol 223 (5) ◽  
pp. 1178-1183 ◽  
Author(s):  
WM Deen ◽  
CR Robertson ◽  
BM Brenner
Keyword(s):  
Glomerular Ultrafiltration

scholarly journals The complex role of nitric oxide in the regulation of glomerular ultrafiltration

2002 ◽  
Vol 61 (3) ◽  
pp. 782-785 ◽  
Author(s):  
Roland C. Blantz ◽  
Aihua Deng ◽  
Mark Lortie ◽  
Karen Munger ◽  
Volker Vallon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glomerular Ultrafiltration

scholarly journals Mechanisms of the defect in glomerular ultrafiltration associated with gentamicin administration

1977 ◽  
Vol 12 (5) ◽  
pp. 344-353 ◽  
Author(s):  
Christine Baylis ◽  
Helmut R. Rennke ◽  
Barry M. Brenner
Keyword(s):  
Glomerular Ultrafiltration

DIFFERENTIAL NEURAL CONTROL OF GLOMERULAR ULTRAFILTRATION

2004 ◽  
Vol 31 (5-6) ◽  
pp. 380-386 ◽  
Author(s):  
Kate M Denton ◽  
Susan E Luff ◽  
Amany Shweta ◽  
Warwick P Anderson
Keyword(s):  
Neural Control ◽  
Glomerular Ultrafiltration

Ultrafiltration of renin in the mouse kidney studied by inhibition of tubular protein reabsorption with lysine

1988 ◽  
Vol 75 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Ingrid Mazanti ◽  
Kirstine Lintrup Hermann ◽  
Arne Høj Nielsen ◽  
Knud Poulsen
Keyword(s):  
Intraperitoneal Injection ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Basic Amino Acid ◽  
Tubular Reabsorption ◽  
Renal Tubules ◽  
Plasma Renin Concentration ◽  
Protein Reabsorption ◽  
Glomerular Ultrafiltration

1. In order to study the role of the kidney in the elimination of endogenous plasma renin, renin was measured in the plasma and urine of female mice. 2. The renin concentration was two orders of magnitude lower in urine than in plasma, but it increased after intraperitoneal injection of submandibular mouse renin. No correlation between the plasma renin concentration and the urinary renin concentration and renin excretion rate could be demonstrated. 3. Blockade of the tubular reabsorption of proteins by intraperitoneal injection of the basic amino acid lysine increased the urinary renin concentration, renin excretion rate and renin clearance two to three orders of magnitude, without affecting the plasma renin concentration. 4. This finding demonstrates that ultrafiltered renin is reabsorbed almost completely in the renal tubules and that the mechanism most likely is the same as for other filtered proteins. 5. The large renal renin clearance obtained after intraperitoneal lysine is in accordance with a major role of the kidneys in the elimination of renin from the circulation, by a glomerular ultrafiltration and tubular reabsorption and metabolization of renin.

Evidence for glomerular actions of ADH and dibutyryl cyclic AMP in the rat

1977 ◽  
Vol 233 (2) ◽  
pp. F102-F117
Author(s):  
I. Ichikawa ◽  
B. M. Brenner
Keyword(s):  
Cyclic Amp ◽  
Arginine Vasopressin ◽  
Urine Flow ◽  
Hydraulic Pressure ◽  
Dibutyryl Cyclic Amp ◽  
Water Diuresis ◽  
Single Nephron ◽  
Arterial Hemorrhage ◽  
Glomerular Ultrafiltration ◽  
Stimulation Of

Experiments were performed on 54 chronically water diuretic Munich-Wistar rats to investigate the effects of various antidiuretic peptides on the determinants of glomerular ultrafiltration. Transition from water diuresis to antidiuresis, induced either by intravenous infusion of 1) exogenous peptides (Pitressin, synthetic arginine vasopressin, or synthetic [1-deamino,4-valine]-8-D-arginine vasopressin) or 2) dibutyryl cyclic AMP, or by stimulation of endogenous ADH release by acute, mild arterial hemorrhage, was associated with near-constant or decreased values for single nephron (SN) and total kidney GFR. Nevertheless, the glomerular transcapillary hydraulic pressure difference (deltaP) uniformly increased with antidiuresis, due to consistent reductions in Bowman's space hydraulic pressure rather than to increases in glomerular capillary hydraulic pressure, the former a consequence of the fall in urine flow rate. In all antidiuretic states, the rats were uniformly observed to be at filtration pressure disequilibrium, permitting calculation of unique values of the glomerular ultrafiltration coefficient (Kf). These values of Kf in antidiuresis were invariably lower than the values obtained during water diuresis. Whether these effects of ADH and DBcAMP on deltaP and Kf represent physiological influences in the control of GFR remains uncertain; their offsetting effects in the present studies usually failed to alter GFR appreciably.

Glomerular effects of angiotensin II require intrarenal factors

1990 ◽  
Vol 258 (3) ◽  
pp. F717-F721 ◽  
Author(s):  
T. B. Wiegmann ◽  
M. L. MacDougall ◽  
V. J. Savin
Keyword(s):  
Angiotensin Ii ◽  
Rate Of Change ◽  
Ang Ii ◽  
Membrane Area ◽  
Isolated Glomeruli ◽  
Systemic Factors ◽  
Glomerular Ultrafiltration

Glomerular ultrafiltration coefficient (Kf) of glomeruli isolated from kidneys of normovolemic rats decreases following infusion of angiotensin II (ANG II). Kf from isolated glomeruli after ANG II infusion in vivo and from isolated perfused kidneys following infusion of ANG II in vitro was measured to determine whether the decrease required the presence of systemic factors. Filtration was induced in vitro and the maximum rate of change in glomerular volume was used to calculate Kf. Glomerular capillary hydraulic conductivity (Lp) was calculated from Lp = Kf/A where the basement membrane area A was calculated as 3 X pi X D2. ANG II infusion in vivo in rats diminished Lp from 3.19 +/- 0.19 to 1.96 +/- 0.13 and to 1.82 +/- 0.11 microliters.min-1.mmHg-1.cm-2, respectively. ANG II infusion into isolated kidneys caused a similar decrease in Lp (3.55 +/- 0.11 to 2.37 +/- 0.07). ANG II infusion either in vivo or during isolated kidney perfusion decreases Kf and Lp. ANG II effects do not require the presence of extrarenal factors but depend on perfusion in situ since incubation of isolated glomeruli with ANG II did not alter Kf.

ANF inhibits vasopressin-induced Ca2+ mobilization and contraction in glomerular mesangial cells

1988 ◽  
Vol 255 (4) ◽  
pp. F771-F780 ◽  
Author(s):  
H. Meyer-Lehnert ◽  
P. Tsai ◽  
C. Caramelo ◽  
R. W. Schrier
Keyword(s):  
Glomerular Filtration ◽  
Contractile Response ◽  
Mesangial Cells ◽  
Second Messenger ◽  
Glomerular Mesangial Cells ◽  
Imaging Analysis ◽  
Cell Contraction ◽  
Filtration Area ◽  
Glomerular Ultrafiltration

It has been suggested that atrial natriuretic factor (ANF) may increase glomerular filtration rate (GFR) via alteration of the glomerular ultrafiltration area, which is at least in part regulated by the contractile state of mesangial cells. The present study therefore investigated the effect of ANF (atriopeptin III) on arginine vasopressin (AVP)-induced Ca2+ mobilization and contraction in cultured rat mesangial cells. AVP (10(-8) M) increased intracellular Ca2+ ([ Ca2+]i) as measured by the quin2 method (142.1 +/- 3.7 vs. 297.9 +/- 8.9 nM, P less than 0.001). This effect, however, was diminished by 10(-8) M ANF (297.9 +/- 8.9 vs. 233.1 +/- 9.3 nM, P less than 0.0025). ANF alone did not affect basal [Ca2+]i. AVP-stimulated 45Ca2+ efflux (cpm.mg prot-1.30 s-1) from mesangial cells within 30 s (1,432 +/- 70 basal vs. 2,751 +/- 287 AVP at 30 s, P less than 0.001). This effect of AVP on 45Ca2+ efflux was also inhibited by ANF (1,403 +/- 62 basal vs. 1,584 +/- 87 AVP and ANF, NS); ANF alone had no effect on spontaneous 45Ca2+ efflux. Furthermore, ANF inhibited AVP-induced 45Ca2+ uptake, which is purportedly one of the major determinants of the sustained phase of cell contraction. Cell contraction was assessed by digital imaging analysis. AVP (10(-7) M) caused contraction of 33.8 +/- 2.0% of the cells, but the contractile response decreased to 20.7 +/- 2.3% in the presence of 10(-9) M ANF and was virtually abolished in the presence of 10(-8) M ANF. Guanosine 3',5'-cyclic monophosphate (cGMP) has been proposed as the second messenger for ANF. ANF (10(-7) M) stimulated cGMP production significantly (0.54 +/- 0.12 vs. 22.30 +/- 5.91 pmol.mg prot-1.10 min-1, P less than 0.01), but it had no effect on cGMP at concentrations of 10(-8) M and below. 8-Bromo-cGMP (8-BrcGMP) attenuated the stimulatory effect of AVP on [Ca2+]i, 45Ca2+ efflux, and 45Ca2+ uptake. AVP-induced cell contraction was also decreased in the presence of 2 mM 8-BrcGMP (33.8 +/- 2.0% vs. 18.8 +/- 2.6%, P less than 0.005). The present results suggest that ANF may increase GFR in part by blocking the cellular action of AVP and possibly other vasoconstrictors on glomerular mesangial cells, thus affecting glomerular filtration area. A role of cGMP as second messenger for ANF is possible, but it appears unlikely to be the only mediator for the effects of ANF.

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