Evolution of adrenal-regeneration hypertension in blinded rats.

The influence of blinding upon the blood pressure and adrenal regeneration of monoephrectomized but otherwise normal and mononephrectomized adrenal-enucleate rats on a high Na intake was evaluated. Blinding had no effect on control blood pressure, or upon the incidence, course and severity of adrenal-regeneration hypertension. Similarly there was no discernible effect on the regeneration of enucleate adrenal glands. The adrenal glandsands of otherwise normal blinded rats showed some enlargement in proportion to body weight, a finding which is probably attributable to loss of body weight in several animals.

Effects of prostaglandin E2 and prostaglandin inhibitors on adrenal regeneration hypertension.

The effects of prostaglandin E2 (PGE2) and a prostaglandin inhibitor, indomethacin, on the development of adrenal regeneration hypertension (ARH) were investigated. Weanling female rats underwent right adrenonephrectomy and left adrenal enucleation. PGE2 was injected subcutaneously daily in dosages of 0, 20, 40 and 80 mug/day. Indomethacin, 1 mg/kg, was administered twice daily by gavage. Blood pressures were determined by a tail and cuff plethysmographic method at 3, 5, and 7 wk after surgery. Increases in dosage of PGE2 produced a progressive reduction in mean blood pressures, heart, and kidney weights. Indomethacin produced significant increases in mean blood pressure, heart, kidney, and adrenal weights. The effects of aspirin and indomethacin on the blood pressures of rats with right adrenalectomy, left adrenal enucleation, and intact kidneys were studied. Administration of asprin twice daily (25 or 50 mg/kg) produced a fall in blood pressure, body and heart weight. Administration of 1 mg/kg twice daily of indomethacin resulted in a significant increase in blood pressure at 3 wk, and 0.1 or 1 mg/kg caused significant increases at 5 wk. The heart, kidney, and adrenal weights also showed increases with indomethacin administration. This study suggests that a deficiency of renal PGE2 may be involved in the etiology of ARH.