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Biomedical subjects

J Ofstad

Publications and source records attributed to J Ofstad.

At least 37 records · Page 2Linked to original sources
PubMed1988

Effect of fasting on lysosomes in kidney cortex of glomerulonephritic rats.

The effect of food restriction (FR) on the kidney cortex lysosomes prepared by rate and isopycnic zonal centrifugation was studied in rats with passive Heymann glomerulonephritis (PHN). FR reduced the renal mass by 41%, but the capacity for handling of labelled endocytosed proteins by the lysosomes was not different from fed PHN rats. While PHN with heavy proteinuria increased the recovery of lysosomal enzymes in the large lysosomes located in the proximal tubule, no changes were observed in FR-PHN rats in spite of significant proteinuria. The density of the small lysosomes was significantly shifted/reduced (from 1,200 and 1,235 g/ml to 1,185 and 1,225 g/ml, respectively) in both fed and FR-PHN rats, suggesting that the handling of extra loads of protein may enhance the absorptive function of small lysosomes found in the lower part of the nephron. FR reduced the mechanical fragility of lysosomes in the kidney cortex of PHN-rats. The highly increased urinary excretion of lysosomal enzymes in fed PHN rats was not observed in FR-PHN rats. As a conclusion, FR reduces both the fragility of lysosomes and the proportion of digestive enzymes in fragile lysosomes. These lysosomal enzymes may be of pathogenic importance in PHN causing cell damage when liberated from disrupted lysosomes.

Animals↗
PubMed1988

Loss of renal blood flow autoregulation in chronic glomerulonephritic rats.

Autoregulation of renal blood flow (RBF) was investigated in subacute (2 mo) and chronic (18 mo) passive Heymann nephritis (PH-2, PH-18) and age-matched controls (C-2, C-18). RBF was significantly lower in PH-18 than in C-18 (3.7 +/- 0.4 vs. 4.7 +/- 0.5 ml.min-1.kidney-1; P less than 0.05), whereas the mean blood pressure (MAP) was similar. The creatinine clearance was significantly lower in PH-18 than in C-18 (1.89 +/- 0.5 vs. 3.15 +/- 0.77 ml.min-1.kg body wt-1; P less than 0.002). Kidney weight was significantly higher in PH-18 than in C-18 (P less than 0.002). In PH-2 and C-2, RBF, MAP, creatinine clearance, and kidney weight were not different (P greater than 0.10). In PH-18 the maximal reduction of the renal vascular resistance (RVR) during RBF autoregulation was 4 +/- 2%, compared with 24 +/- 4% in C-18 (P less than 0.002); the lower pressure limit of RBF autoregulation was 131 +/- 9 vs. 85 +/- 4 mmHg (P less than 0.002). In PH-2 the maximal reduction of RVR during RBF autoregulation was 18 +/- 3%; in C-2 it was 25 +/- 2% (P greater than 0.10); the lower pressure limit of RBF autoregulation was 101 +/- 4 vs. 84 +/- 6 mmHg (P less than 0.02). It is concluded that RBF autoregulation is nearly lost in the late stage of glomerulonephritis, possibly as a consequence of the nephron loss.

Animals↗
PubMed1987

The effect of hypertension on glomerular structures and capillary permeability in passive Heymann glomerulonephritis.

In glomerulonephritic and normal kidneys hypertension has been shown to increase the urinary protein excretion and the thickness of the glomerular basement membrane and to reduce the glomerular filtration rate. We have studied the effect of desoxycorticosterone acetate (DOCA)-salt hypertension on the glomerular anatomy and function in normal control rats and rats with passive Heymann nephritis. Standard methods for measurements of glomerular filtration rate and urinary protein excretion were used and the results were correlated to morphometrical measurements in randomly selected glomeruli in all groups. In control rats, DOCA-salt hypertension increased the kidney weight (P less than 0.001), the glomerular volume (P less than 0.05), and the surface of peripheral glomerular basement membrane (P less than 0.01). The thickness of peripheral glomerular basement membrane and the length of glomerulary capillaries were not affected. In glomerulonephritic rats, DOCA-salt hypertension did not change the kidney weight and glomerular capillary diameter. The thickness of the peripheral basement membrane increased (P less than 0.05), while the length of glomerular capillaries and the surface of peripheral basement membrane were reduced (P less than 0.05). Glomerular filtration rate per unit peripheral basement membrane was not significantly different among the groups while protein excretion per unit peripheral basement membrane increased significantly both in the hypertensive and in the glomerulonephritic groups. The estimated hydraulic conductivity of the glomerular capillaries was reduced both in rats with DOCA-salt hypertension and glomerulonephritic rats with and without DOCA-salt hypertension. In conclusion, DOCA-salt hypertension seems to decrease hydraulic conductivity and increase protein excretion both in normal and in glomerulonephritic kidneys although the effect on glomerular morphology is different.

Animals↗
PubMed1987

Autoregulation of renal blood flow (RBF) with and without participation of afferent arterioles.

The participation of the afferent arterioles (AA) in RBF autoregulation was studied in two groups of rats (groups A and B) by measurement of the afferent arteriolar diameters (dAA) by the microsphere method at control pressure (groups A and B), at the lower pressure limit of RBF autoregulation (group A) and at a perfusion pressure half-way between these pressures (intermediate pressure) (group B). The RBF was autoregulated from 109 +/- 7 (control pressure) to 80 +/- 7 mmHg (lower pressure limit) in group A, and from 101 +/- 4 (control pressure) to 77 +/- 3 mmHg in group B. In group A, dAA was significantly lower (17.2 +/- 0.3 micron) at control pressure than at the lower pressure limit of RBF autoregulation (20.3 +/- 0.03 micron) (P less than 0.005). In group B, dAA was 17.3 +/- 0.3 micron at control pressure and 17.1 +/- 0.4 micron at the intermediate pressure (89 +/- 3 mmHg) (P greater than 0.10). The results indicate that dilation of the afferent arterioles occurs only in the lower part of the autoregulatory pressure range. Possibly, RBF autoregulation at minor pressure reductions is achieved by dilation of the interlobular artery. Participation of the glomerular hilar branches of the afferent arterioles in RBF autoregulation cannot be excluded.

Animals↗
PubMed1987

Resetting of renal blood flow autoregulation in spontaneously hypertensive rats.

Renal blood flow (RBF) autoregulation was examined in untreated 10- and 40-wk-old spontaneously hypertensive rats (SHR) [mean arterial pressure (MAP) 125 +/- 4 and 167 +/- 7 mmHg] and in captopril-treated (7 days) 10- and 40-wk-old SHR (88 +/- 7 and 112 +/- 5 mmHg). Age-matched Wistar-Kyoto rats (WKY) were used as controls (MAP 91 +/- 3 and 104 +/- 2 mmHg). The study was carried out in rats with and without acute uninephrectomy. In 10-wk-old acutely uninephrectomized animals, the lower pressure limit of autoregulation was 78 +/- 4 mmHg in WKY, 102 +/- 5 mmHg in SHR (P less than 0.02), and 78 +/- 7 mmHg in captopril-treated SHR (P greater than 0.10). The renal vascular resistance (RVR) was significantly elevated at the lower pressure limit of RBF autoregulation in untreated SHR (P less than 0.02) but became normal after treatment (P greater than 0.10). Neither uninephrectomy nor variation of RBF between different batches seemed to influence the lower pressure limit of RBF autoregulation. In 40-wk-old acutely nephrectomized animals, the lower pressure limit of RBF autoregulation in WKY was 85 +/- 4 mmHg, 128 +/- 3 mmHg in SHR (P less than 0.001), and 101 +/- 5 mmHg in captopril-treated SHR (P less than 0.01). RVR at the lower pressure limit was increased in untreated SHR (P less than 0.01), but fell to normal values during captopril treatment. Neither the uninephrectomy nor variation of RBF between different batches of rats seemed to influence the lower pressure limit of RBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Changes in lysosome populations in the rat kidney cortex induced by passive Heymann glomerulonephritis.

Acute passive Heymann glomerulonephritis in rats induced heavy proteinuria and highly increased urinary activity of N-acetyl-beta-D-glucosaminidase, acid beta-galactosidase and acid phosphatase. The cortical activity of these acid hydrolases was increased essentially in the large lysosomes as demonstrated by subfractionation of the lysosome-rich mitochondrial-lysosomal fraction, by rate zonal centrifugation. Banding density of small lysosomes shifted or reduced to slightly lower value (1.225 g/ml), which is between the banding densities of small 'light' (1.20 g/ml) and small 'dense' lysosomes (1.235 g/ml) in normal rat kidney cortex. Labelled protein reabsorbed in the proximal tubule is recovered in these populations of small lysosomes as well as in the large lysosomes or 'protein droplets'. Glomerulonephritis also induced a new population of small 'light' lysosomes (density 1.185-1.195 g/ml) enriched in cathepsin D. The previously demonstrated morphological, biochemical, and physiological heterogeneity of renal lysosomes was confirmed and emphasized in the kidney cortex of glomerulonephritic rats. The main changes in the lysosomal populations appear to reflect the increased protein reabsorption as confirmed by the proteinuria.

Acetylglucosaminidase↗
PubMed1986

Analytical study of kallikrein and kallikrein-like esterase activity in subfractions from rat kidney cortex microsomes and isolated subcellular membranes.

Heavy and light microsomal fractions were subfractioned using high performance zonal rotors, and assayed for apoprotenin sensitive kallikrein-like amidolytic activity (pH 8.2). The activity profiles for the various substrates assayed show rather complex distribution pattern demonstrating kallikrein-like amidolytic activity in plasma membranes, basolateral membranes, rough endoplasmic reticulum and membranes derived from the Golgi complex.

Aminopeptidases↗
PubMed1986

Autoregulation of renal blood flow in two-kidney, one-clip hypertensive rats.

Renal blood flow (RBF) autoregulation was examined in the clipped and nonclipped kidneys in two groups of two-kidney, one-clip (2K-1C) hypertensive rats 10 wk after clipping. The arterial pressure distal to the clip and the renin secretion rate (RSR) were also examined. The blood pressure (BP) was 149 +/- 4 and 162 +/- 6 mmHg in the two hypertensive groups vs. 114 +/- 3 mmHg in the controls (P less than 0.02). The RBF (in ml X min-1 X kidney-1) was 4.27 +/- 0.41 in the nonclipped and 2.18 +/- 0.23 in the clipped kidneys (P less than 0.001). The pressure distal to the clip was 104 +/- 7 mmHg. The renal vascular resistance (RVR) (in mmHg X ml-1 X min-1 X g-1) was 25.0 +/- 1.4 in the control kidneys vs. 58.4 +/- 4.5 in the nonclipped (P less than 0.001) and 39.9 +/- 6.6 in the clipped kidneys (P less than 0.01). The RBF autoregulation was well preserved in the nonclipped kidneys but reset to a higher lower pressure limit of autoregulation of 106 +/- 4 mmHg, which was significantly higher than in the normotensive controls (84 +/- 6 mmHg) (P less than 0.01). In the clipped kidneys there was complete loss of RBF autoregulation. RSR decreased with reduction of the perfusion pressure in the clipped kidneys. The increased RVR might have been due to a combination of structural and functional changes in both kidneys.

Animals↗
PubMed1984

Interstitial colloid osmotic and hydrostatic pressures in human subcutaneous tissue during early stages of heart failure.

Subcutaneous oedema is a common finding in heart failure. However, some patients have reduced cardiac pump function without oedema. The aim of this study was to investigate whether local mechanisms in subcutaneous tissue contribute to oedema prevention. A reduction in interstitial colloid osmotic pressure (pii) and a rise in interstitial fluid hydrostatic pressure (Pi) will both counteract a rise in capillary filtration caused by heart failure. Cardiac catheterization was done in 22 angina pectoris patients without visible oedema. Two days later pii was measured with a wick method and Pi was measured with a wick-in-needle method. Both parameters were measured in subcutaneous tissue on thorax at heart level and on the ankle. Plasma volume was determined by 125I-albumin and extracellular volume measured with 35SO4. Parameters of cardiac pump function ranged from normal to clearly pathological values. Mean pii was 13.0 mmHg on thorax and 8.3 mmHg on the ankle. Pi averaged -2.1 mmHg on thorax and -1.5 mmHg on the ankle. Statistically significant (P less than 0.05) correlations were found between pii on thorax and left ventricular end diastolic pressure (rs -0.40) and pii on thorax and cardiac index (rs 0.42). Pi was positively correlated to right atrial pressure (rs 0.50). Body fluid volumes were normal or moderately reduced. The study shows that a reduction in cardiac pump function is associated with a reduction in pii and a rise in Pi. These changes may help to prevent oedema formation in the early stages of heart failure.

Adult↗
PubMed1984

Effect of hypertension on experimental glomerulonephritis in rats.

The effect of hypertension on the anatomy, physiology, and course of glomerulonephritis in rats was investigated by inducing deoxycorticosterone acetate-salt hypertension in animals with heterologous immune complex glomerulonephritis and vice versa. The effect of hypertension on glomerulonephritis with different degrees of intensity was also studied. Hypertension increased the proteinuria in the glomerulonephritic rat substantially (p less than 0.01), reduced the creatinine clearance (p less than 0.05), and induced an enormous thickening of the glomerular basement membrane. Furthermore, the life span was shortened (p less than 0.01) when hypertension was induced in nephritic rats, possibly due to insufficient cerebral vascular activity secondary to malnutrition. Glomerulonephritis did not influence the blood pressure in animals with severe protein loss; in rats with minor proteinuria the presence of glomerulonephritis increased the blood pressure. Hypertension lowered the antiserum dose needed to produce pathologic proteinuria (p less than 0.02). Hypertension seemed to increase the amount of glomerular immune deposits in early glomerulonephritis but lowered the amounts of glomerular rat IgG during the course of nephritis. In conclusion, hypertension increases the glomerular damage substantially in rats with heterologous immune complex glomerulonephritis, influences the glomerular deposition of immunoglobulins, and shortens the life span.

Animals↗
PubMed1983

Afferent arteriolar diameter in DOCA-salt and two-kidney one-clip hypertensive rats.

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.

Animals↗
PubMed1982

The heterologous immune complex glomerulonephritis. A dose dependent glomerulonephritis with acute, latent and chronic phases in a long-term study.

The pathophysiology, histology and immunohistology of acute and chronic heterologous immune complex glomerulonephritis were investigated in a long-term study in male Wistar rats. The glomerulonephritis showed 3 phases: an initial nephrotic syndrome, a latent phase with stable proteinuria (40 mg/24 h), and a terminal phase with increasing proteinuria and blood pressure, and declining serum protein concentration and creatinine clearance. Antiserum doses of 1.0, 1.5 and 2.0 ml induced maximal proteinuria (112, 257 and 272 mg/24 h respectively) after 14 days whereas normal rabbit serum and 0.5 ml antiserum gave no proteinuria. After 100 days, the rats injected with 1.0 ml of antiserum did not show physiological signs of renal disease; in the rats injected with 1.5 ml of antiserum the disease run a chronic course. Equal amounts of rabbit IgG, rat IgG and rat C3 were found in 10 glomeruli from rats 100 days after injection of 0.5, 1.0 and 2.0 ml (p greater than 0.10). Intramembranous deposits and spike formation were observed in all groups. All changes increased with greater antiserum doses. Chronically diseased animals observed from 500 to 750 days showed deposits of rabbit IgG in the basement membrane, and in most animals small amounts of rat IgG and rat C3 were also observed. This is compatible with a sustained stimulus for antibody formation throughout the course of this type of glomerulonephritis.

Acute Disease↗