Calcium Carbonate Exacerbates Glomerular Capillary Hypertension and Injury in Rats With Desoxycorticosterone-salt Hypertension

1990 ◽  
Vol 3 (6 Pt 1) ◽  
pp. 444-450 ◽  
Author(s):  
L. D. Dworkin ◽  
H. D. Feiner ◽  
M. Parker ◽  
J. Randazzo
Keyword(s):  
Calcium Carbonate ◽  
Glomerular Capillary ◽  
Salt Hypertension ◽  
Glomerular Capillary Hypertension

scholarly journals Anemia ameliorates progressive renal injury in experimental DOCA-salt hypertension.

1991 ◽  
Vol 1 (10) ◽  
pp. 1180-1185
Author(s):  
H M Lafferty ◽  
D L Garcia ◽  
H G Rennke ◽  
J L Troy ◽  
S Anderson ◽  
...  
Keyword(s):  
Recombinant Human Erythropoietin ◽  
Glomerular Sclerosis ◽  
Glomerular Injury ◽  
Glomerular Capillary ◽  
Human Erythropoietin ◽  
Glomerular Hypertension ◽  
Salt Hypertension ◽  
Contrast Reduction ◽  
Glomerular Capillary Hypertension

To explore the role of systemic hematocrit in the vascular adaptations which characterize desoxycorticosterone-salt hypertension, studies were performed in three groups of rats with uninephrectomy, desoxycorticosterone administration, and 1% saline in the drinking water. One group received recombinant human erythropoietin to increase hematocrit, and another group was subjected to phlebotomy and fed a low-iron diet to induce anemia. Control rats exhibited systemic and glomerular capillary hypertension, proteinuria, and substantial glomerular sclerosis at 8 wk. Erythropoietin modestly increased hematocrit and blood pressure and substantially aggravated glomerular capillary pressure, proteinuria, and glomerular sclerosis. In contrast, reduction of hematocrit with a low-iron diet significantly attenuated systemic and glomerular hypertension, proteinuria, and sclerosis. It was concluded that the pace of progression of glomerular injury can be limited by chronic reduction in hematocrit, which effectively ameliorates both systemic and glomerular hypertension in this model of salt-sensitive hypertensive renal disease.

Effects of nifedipine and enalapril on glomerular injury in rats with deoxycorticosterone-salt hypertension

1990 ◽  
Vol 259 (4) ◽  
pp. F598-F604 ◽  
Author(s):  
L. D. Dworkin ◽  
R. I. Levin ◽  
J. A. Benstein ◽  
M. Parker ◽  
M. E. Ullian ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Severe Hypertension ◽  
Calcium Entry Blocker ◽  
Glomerular Injury ◽  
Kidney Weight ◽  
Inhibition Of Platelet Aggregation ◽  
Glomerular Capillary ◽  
Salt Hypertension ◽  
Glomerular Lesions ◽  
And Control

Male Munich-Wistar rats underwent right nephrectomy and were given weekly injections of deoxycorticosterone acetate (DOCA) and 1% saline (salt) to drink. Two studies were performed. In the first, rats given enalapril (ENP) were compared with controls. In the second, rats ingested either standard chow or chow to which the calcium-entry blocker nifedipine (NIF) had been added. Six to eight weeks after nephrectomy, both control DOCA-salt rats and those given ENP had severe hypertension and significant proteinuria. Rats given NIF excreted less protein, and glomerular lesions were not observed in this group. The effects of NIF on several parameters that have been associated with glomerular injury were examined. Micropuncture studies revealed that glomerular capillary pressure was increased in DOCA-salt rats and was not reduced by NIF. Platelet aggregation was also similar in NIF-treated and control rats. Morphometric studies revealed a tendency toward lower glomerular volume of NIF-treated rats; however, kidney weight and glomerular capillary radius were unaffected by therapy. Thus NIF, but not ENP, prevents DOCA-salt rats from developing hypertension and glomerular injury. This effect does not depend on reduction in glomerular pressure or inhibition of platelet aggregation.

Abstract MP46: Knockout Of Add3 Impairs Autoregulation Of Renal Blood Flow And Promotes Hypertension-induced Renal Injury By Increasing Glomerular Capillary Pressure And Podocyte Loss

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Letao Fan ◽  
Wenjun Gao ◽  
Yedan Liu ◽  
Bond V Nguyen ◽  
Joshua R Jefferson ◽  
...  
Keyword(s):  
Capillary Pressure ◽  
Renal Injury ◽  
Time Course ◽  
Interstitial Fibrosis ◽  
Myogenic Response ◽  
Mesenchymal Transition ◽  
Glomerular Capillary ◽  
Glomerular Capillary Pressure ◽  
Podocyte Loss ◽  
Salt Hypertension

Recently, we reported that a mutation in γ-Adducin (ADD3) alters the actin cytoskeleton and is associated with an impaired myogenic response of the afferent arteriole and enhanced hypertension-induced renal disease. However, it remains to be determined whether the loss of ADD3 function promotes renal injury by increasing glomerular capillary pressure (Pgc) and podocyte loss or other mechanisms. The present study compared the time course of changes in renal hemodynamics and the progression of renal injury during the development of DOCA-salt hypertension in FHH 1 BN rats (WT) with an intact myogenic response vs. FHH 1 BN Add3KO rats (Add3KO) in which the myogenic response is impaired. When transmural pressure rose from 40 to 100 mmHg, the inner diameter of the preglomerular artery constricted by 19% (47.7 ± 4.3 to 38.4 ± 3.4 μm, n = 5) in WT, but it dilated by 28% (53.0 ± 2.2 to 67.9 ± 4.3 μm, n = 7) in Add3KO. Pgc was similar (50.1 ± 0.4 vs. 51.2 ± 0.8 mmHg, n = 6) at 100 mmHg, but rose by 6 and 14 mmHg in WT vs. Add3KO when perfusion pressure rose to 150 mmHg. Mean arterial pressure increased similarly and reached 177.7 ± 3.5 vs. 182.6 ± 2.3 mmHg (n = 9) after 3 weeks of DOCA-salt hypertension in WT vs. Add3KO. After 1 week of DOCA-salt hypertension, glomerular filtration rate (GFR) increased by 38% (1.2 ± 0.1 to 1.6 ± 0.1 ml/min/kidney, n = 6) and glomerular nephrin expression decreased by 20% (165.4 ± 4.5 to 131.614 ± 5.2 RFU, n = 7) in Add3KO. Both were unaltered in WT. Proteinuria increased 2 folds in WT (56.9 ± 4.7 to 168.6 ± 26.7 mg/day, n = 12) in the first week of hypertension vs. a 6-fold increase in Add3KO (64.6 ± 4.1 to 446.0 ± 41.9 mg/day, n = 9). After 3 weeks of hypertension, the degree of glomerulosclerosis (3.4 ± 0.1 vs. 2.4 ± 0.1 glomerular injury score, n = 9~12), protein cast formation (9.0% ± 0.8% vs. 4.8% ± 0.4% of area, n = 6), epithelial-mesenchymal transition, interstitial fibrosis (17.9% ± 0.8% vs. 9.5% ± 0.3% of area, n = 6), and inflammation was significantly greater in Add3KO vs. WT. GFR and Pgc were 28% and 19% lower in Add3KO than WT. These results indicate that the impaired myogenic response increases the transmission of pressure to the glomerulus to induce the loss of podocytes, which accelerates the progression of renal injury during the development of hypertension in Add3KO.

Physiological and structural responses to chronic experimental renal allograft injury

1994 ◽  
Vol 267 (6) ◽  
pp. F1102-F1106 ◽  
Author(s):  
A. Junaid ◽  
S. M. Kren ◽  
M. E. Rosenberg ◽  
K. A. Nath ◽  
T. H. Hostetter
Keyword(s):  
Chronic Rejection ◽  
Renal Allograft ◽  
Donor Organ ◽  
Glomerular Capillary ◽  
Protein Excretion ◽  
Interstitial Volume ◽  
Number Of Patients ◽  
Injury Mechanisms ◽  
Structural Responses ◽  
Glomerular Capillary Hypertension

Chronic rejection necessitates a return to dialysis or retransplantation for a significant number of patients with renal allografts. Although alloresponses between donor organ and recipient importantly determine this process, the detailed immunologic processes and organ physiology of chronic rejection are unclear; in consequence its mechanism and therapy are uncertain. A model of chronic rejection in the rat was used to examine several facets of this process. Fisher-to-Lewis (F-L), allogeneic, and Lewis-to-Lewis (L-L), syngeneic, renal transplants were performed in nephrectomized recipients. All rats were treated with cyclosporin A (5 mg.kg-1.day-1) for 10 days from the time of grafting. At 6 wk, allogeneically grafted animals had a higher protein excretion rate (F-L, 47 +/- 30 mg/day; L-L, 17 +/- 6 mg/day; P <0.05) and an increase in glomerular capillary pressure (F-L, 69 +/- 5 mmHg; L-L, 58 +/- 8 mmHg; P <0.05) and fractional cortical interstitial volume (F-L, 29.8 +/- 4.3%; L-L, 19.5 +/- 4.0%; P < 0.01). This model of chronic rejection is characterized by glomerular capillary hypertension, proteinuria, and cortical interstitial expansion. Because these findings are also present in other models of chronic renal injury, mechanisms in addition to alloresponses may operate in chronic rejection.

scholarly journals Pathogenesis of glomerular injury in the fawn-hooded rat: early glomerular capillary hypertension predicts glomerular sclerosis.

1993 ◽  
Vol 3 (11) ◽  
pp. 1775-1782 ◽  
Author(s):  
J L Simons ◽  
A P Provoost ◽  
S Anderson ◽  
J L Troy ◽  
H G Rennke ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Rapid Development ◽  
Systemic Hypertension ◽  
Glomerular Sclerosis ◽  
Hydraulic Pressure ◽  
Glomerular Capillary ◽  
Morphological Studies ◽  
Glomerular Capillary Hypertension ◽  
Segmental Glomerular Sclerosis

Fawn-hooded rats spontaneously develop focal and segmental glomerular sclerosis, systemic hypertension, and proteinuria at a young age. Micropuncture and morphological studies were performed in two inbred strains of fawn-hooded rats, FHH and FHL, with different susceptibilities to develop chronic renal failure. FHH rats have higher values for systolic blood pressure and proteinuria and more rapid development of focal and segmental glomerular sclerosis and subsequent chronic renal failure as compared with genetically closely related FHL rats. FHH and FHL strains and a Wistar control strain, WAG, were matched for age and were studied at 16 wk. FHH, FHL, and WAG-old (WAG-O) strains were matched for weight, and the last group was studied at 22 wk. WAG were also matched for weight to a young group of FHH rats (FHH-Y), and these were studied at 8 wk. In comparison with WAG and WAG-O rats, FHH and FHH-Y rats exhibited an increased in mean glomerular capillary hydraulic pressure (WAG, 52 +/- 1 mm Hg; WAG-O, 47 +/- 2 mm Hg; FHH, 60 +/- 2 mm Hg; FHH-Y, 65 +/- 1 mm Hg), whereas values in FHL animals were intermediate (56 +/- 2 mm Hg). No significant differences in glomerular volume were found among groups. Moderate focal and segmental glomerular sclerosis developed in FHH and FHH-Y rats, with values for older FHH rats being significantly greater than those for WAG, WAG-O, and FHL animals. Thus, the genetically determined sensitivity to develop proteinuria, focal and segmental glomerular sclerosis, and chronic renal failure in fawn-hooded rats correlated with early evidence of glomerular capillary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanical strain increases SPARC levels in podocytes: implications for glomerulosclerosis

2005 ◽  
Vol 289 (3) ◽  
pp. F577-F584 ◽  
Author(s):  
Raghu V. Durvasula ◽  
Stuart J. Shankland
Keyword(s):  
Spontaneously Hypertensive Rat ◽  
Mechanical Strain ◽  
Early Event ◽  
Matricellular Protein ◽  
Podocyte Injury ◽  
Whole Cell Lysate ◽  
Cell Lysate ◽  
Glomerular Capillary ◽  
Glomerular Capillary Hypertension ◽  
Cyclical Stretch

Glomerular capillary hypertension is a final common pathway to glomerulosclerosis. Because podocyte loss is an early event in the development of glomerulosclerosis, it is logical that the deleterious effects of glomerular capillary hypertension involve podocyte injury. Yet, the mechanisms by which elevated intraglomerular pressure is translated into a maladaptive podocyte response remain poorly understood. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein activated in various disease states of the podocyte and accelerates renal injury, as evidenced by the milder course of experimental diabetic nephropathy in SPARC-null mice compared with diabetic SPARC wild-type mice. Accordingly, we tested the hypothesis that mechanical strain activates SPARC in podocytes and thus is a putative mediator of podocyte injury in states of intraglomerular capillary hypertension. Conditionally immortalized mouse podocytes were subjected to 10% cyclical stretch while nonstretched cells served as controls. SPARC levels were measured in whole cell lysate and cell media. Immunostaining was performed for SPARC in an experimental model of glomerular capillary hypertension. Our results demonstrate cyclical stretch of podocytes markedly increased SPARC levels in cell lysate, through activation of p38, as well as secreted SPARC. Relevance was shown by demonstrating increased podocyte staining for SPARC in the uninephrectomized spontaneously hypertensive rat. In conclusion, we have made the novel observation that mechanical forces characteristic of states of glomerular capillary hypertension lead to increased levels of SPARC in podocytes. We speculate that the increase in SPARC may be maladaptive and lead to a progressive reduction in podocyte number, thus fueling the future development of glomerulosclerosis.

scholarly journals Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension.

1986 ◽  
Vol 77 (6) ◽  
pp. 1925-1930 ◽  
Author(s):  
R Zatz ◽  
B R Dunn ◽  
T W Meyer ◽  
S Anderson ◽  
H G Rennke ◽  
...  
Keyword(s):  
Diabetic Glomerulopathy ◽  
Glomerular Capillary ◽  
Glomerular Capillary Hypertension

A TEM study of the microstructure of avian eggshells

1992 ◽  
Vol 50 (2) ◽  
pp. 1102-1103
Author(s):  
S. Q. Xiao ◽  
S. Baden ◽  
A. H. Heuer
Keyword(s):  
Electron Microscope ◽  
Calcium Carbonate ◽  
Nucleation And Growth ◽  
Growth Mechanisms ◽  
Shell Surface ◽  
Thin Sections ◽  
Polycrystalline Metals ◽  
Transmission Electron ◽  
Nucleation And Growth Mechanisms

The avian eggshell is one of the most rapidly mineralizing biological systems known. In situ, 5g of calcium carbonate are crystallized in less than 20 hrs to fabricate the shell. Although there have been much work about the formation of eggshells, controversy about the nucleation and growth mechanisms of the calcite crystals, and their texture in the eggshell, still remain unclear. In this report the microstructure and microchemistry of avian eggshells have been analyzed using transmission electron microscope (TEM) and energy dispersive spectroscopy (EDS).Fresh white and dry brown eggshells were broken and fixed in Karnosky's fixative (kaltitanden) for 2 hrs, then rinsed in distilled H2O. Small speckles of the eggshells were embedded in Spurr medium and thin sections were made ultramicrotome.The crystalline part of eggshells are composed of many small plate-like calcite grains, whose plate normals are approximately parallel to the shell surface. The sizes of the grains are about 0.3×0.3×1 μm3 (Fig.l). These grains are not as closely packed as man-made polycrystalline metals and ceramics, and small gaps between adjacent grains are visible indicating the absence of conventional grain boundaries.

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