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.
Iversen
B M
BM
Medical Department A, School of Medicine, University of Bergen, Norway.
Ofstad
J
J
D000818:Animals; D001485:Basement Membrane / Q000473:pathology; D002199:Capillary Permeability; D003900:Desoxycorticosterone; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D006973:Hypertension / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D003900:Desoxycorticosterone