scholarly journals Glomerular injury in uninephrectomized spontaneously hypertensive rats. A consequence of glomerular capillary hypertension.

1986 ◽  
Vol 77 (3) ◽  
pp. 797-809 ◽  
Author(s):  
L D Dworkin ◽  
H D Feiner
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Glomerular Injury ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Glomerular Capillary ◽  
Glomerular Capillary Hypertension

scholarly journals Induction of hemeoxygenase-1 reduces glomerular injury and apoptosis in diabetic spontaneously hypertensive rats

2012 ◽  
Vol 302 (7) ◽  
pp. F791-F800 ◽  
Author(s):  
Ahmed A. Elmarakby ◽  
Jessica Faulkner ◽  
Babak Baban ◽  
Mohamed A. Saleh ◽  
Jennifer C. Sullivan
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Spontaneously Hypertensive Rats ◽  
Organ Damage ◽  
Protective Role ◽  
Glomerular Injury ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cobalt Protoporphyrin ◽  
And Oxidative Stress

Induction of hemeoxygenase-1 (HO-1) lowers blood pressure and reduces organ damage in hypertensive animal models; however, a potential protective role for HO-1 induction against diabetic-induced glomerular injury remains unclear. We hypothesize that HO-1 induction will protect against diabetes-induced glomerular injury by maintaining glomerular integrity and inhibiting renal apoptosis, inflammation, and oxidative stress. Diabetes was induced with streptozotocin in spontaneously hypertensive rats (SHR) as a model where the coexistence of hypertension and diabetes aggravates the progression of diabetic renal injury. Control and diabetic SHR were randomized to receive vehicle or the HO-1 inducer cobalt protoporphyrin (CoPP). Glomerular albumin permeability was significantly greater in diabetic SHR compared with control, consistent with an increase in apoptosis and decreased glomerular nephrin and α3β1-integrin protein expression in diabetic SHR. CoPP significantly reduced albumin permeability and apoptosis and restored nephrin and α3β1-integrin protein expression levels in diabetic SHR. Glomerular injury in diabetic SHR was also associated with increases in NF-κB-induced inflammation and oxidative stress relative to vehicle-treated SHR, and CoPP significantly blunted diabetes-induced increases in glomerular inflammation and oxidative stress in diabetic SHR. These effects were specific to exogenous stimulation of HO-1, since incubation with the HO inhibitor stannous mesoporphyrin alone did not alter glomerular inflammatory markers or oxidative stress yet was able to prevent CoPP-mediated decreases in these parameters. These data suggest that induction of HO-1 reduces diabetic induced-glomerular injury and apoptosis and these effects are associated with decreased NF-κB-induced inflammation and oxidative stress.

scholarly journals Apoptosis and Glomerular Injury After Prolonged Nitric Oxide Synthase Inhibition in Spontaneously Hypertensive Rats

Hypertension ◽  
2001 ◽  
Vol 38 (6) ◽  
pp. 1300-1306 ◽  
Author(s):  
Hidehiko Ono ◽  
Yuko Ono ◽  
Atsuko Takanohashi ◽  
Hiroaki Matsuoka ◽  
Edward D. Frohlich
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Spontaneously Hypertensive Rats ◽  
Glomerular Injury ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Oxide Synthase
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