No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Rabbits*

No abstract available.
Ephedrine* ; Rabbits*

Roles of the nonclipped kidney in the development and maintenance of the high blood pressure in two- kidney, one clip hypertension remain to be defined. It has been known that the pathophysiology of hypertension is different by the presence or absence of the contralateral kidney in renal hypertension. The present study was undertaken to evaluate the effects of intrarenal norepinephrine in the nonclipped kidney exposed to the high blood pressure. Experiments were performed in 7-day two-kidney, one clip Goldblatt hypertensive and sham-operated normotensive rabbits. The basal levels of renal plasma flow and urine flow, and urinary excretion of electrolytes were higher in the nonclipped kidney of two-kidney, one clip Goldblatt hypertensive than in the corresponding kidney of sham-operated normotensive rabbits. Intrarenal infusion of norepinephrine increased renal perfusion resistance, and decreased renal hemodynamics and renal excretory function in a dose-dependent manner in both hypertensive and normotensive rabbits. The renal hemodynamics and excretory responses to intrarenal norepinephrine infusion were attenuated in two-kidney, one clip Goldblatt hypertensive rabbits. The changes by norepinephrine infusion of the renal excretory function were closely correlated with those in glomerular filtration rate or renal plasma flow. These results suggest that the impaired vascular reactivity in the nonclipped kidney is one of the early changes appeared in the course of multifactorial derangements in renal hypertension and that the impairment may be an adaptive response of the kidney to high blood pressure.
Rabbits ; Animals

Renin-angiotensin system is associated with development of diabetic nephropathy. Hyperglycemia is known as a primary etiologic factor about it. Thus, we investigated the effect of high glucose on angiotensin II(ANG II) binding in the primary cultured rabbit renal proximal tubule cells(PTCs). 25 mM glucose(48 hr incubation) induces inhibition of ANG II binding. The high glucose-induced inhibition of ANG II binding was recovered by the removal of glucose, suggesting the role of glucose specificity. High glucose-induced inhibition of ANG II binding was blocked by mepacrine and AACOCF3, phospholipase A2(PLA2) inhibitors. Indomethacin, a cyclooxygenase inhibitor, significantly prevented high glucose-induced inhibition of ANG II binding. However, nordihydroguaiareic acid(NDGA), a lipoxygenase inhibitor, and econazole, a cytochrome P450 epoxygenase inhibitor, did not block the effect of high glucose. This result suggest that cyclooxygenase metabolites of arachidonic acid(AA) released by high glucose are involved in the high glucose-induced inhibition of ANG II binding. Next, we examined the involvement of PKC in the effect of high glucose. Staurosporine, bisindolylmaleimide I, protein kinase C(PKC) inhibitors, and PD 98059, a p44/42 mitogen activated protein kinase(MAPK) inhibitor, significantly blocked high glucose- induced increase of [3H]-AA release and inhibition of ANG II binding. Indeed, 25 mM glucose increased PKC activity from cytosolic to particulate fraction and phosphorylation of p44/42 MAPK. In addition, high glucose increased phosphorylation of p44/42 MAPK and its activation was significantly blocked by PKC inhibitor. In conclusion, high glucose partially inhibits ANG II binding via PKC-MAPK-PLA2 signal pathway in the PTCs.
Rabbits ; Animals

No abstract available.
Rabbits* ; Regeneration*

No abstract available.
Rabbits ; Animals