The renal medulla and mechanisms of hypertension in the spontaneously hypertensive rat

A significant number of offspring from brother-sister matings of NIH-Okamoto-Aoki spontaneously hypertensive rats (SHRs) were found to be normotensive at 20 weeks of age. Over 20% of the animals that were hypertensive at this age had mild-to-moderate unilateral hydronephrosis at the time of sacrifice. In over 90% of the rats that did not develop hypertension spontaneously, ligation of one ureter raised blood pressure above 150 mm Hg within 2 weeks. In those rats made hypertensive by obstructing one ureter and in those that developed hypertension with accompanying naturally occurring hydronephrosis, subcutaneous implants of fragmented renal medulla from unrelated normal rats decreased blood pressure to normotensive levels. In contrast, medullary implants had no significant effect in rats developing hypertension spontaneously without hydronephrosis. Renal inner medullary plasma flow was low in the obstructed kidneys of hydronephrotic hypertensive SHRs but was elevated in the kidneys of nonhydronephrotic hypertensive SHRs. The hypertension in hydronephrotic SHRs appears to be related to an impairment of the antihypertensive function of the renal medulla. Such an impairment of medullary antihypertensive function does not appear to play a significant role in the hypertension in SHRs without hydronephrosis.     

Effects of morphine sulfate on NADPH-cytochrome c reductase and cytochrome P-450 of mouse liver microsomes

Three hr after i.p. administration of a single dose of 30 mg/kg of morphine to male mice, an increase in specific activity of NADPH-cytochrome c reductase by about 10% and the content of cytochrome P-450 by about 14% of their liver microsomes was observed.Administration of 30 mg/kg of morphine, once daily,during 5 days, caused about 16% and 9% increases in specific activity of c reductase and the content of P-450 respectively. Administration of a single dose of morphine to male and female mice caused no sex-dependent differences in the specific activity of c reductase and the content of P-450. Repeated administration of morphine up to 100 mg/kg to male mice increased the specific activity of microsomal c reductase by about 70%. Repeated administration of morphine up to 55 mg/kg also increased the microsomal content of P-450 by about 22%, but with higher doses of morphine, the content of P-450 declined and finally dropped below control levels. The levels of c-reductase activity and P-450 content returned to normal levels about 2 weeks after termination of morphine administration.