Objective      To explore the role of renal angiotensin II type-1 receptor (AT

1

R) in hypertensive offsprings of ra

ts with maternal diabetes and related mechanism.       Methods      Twenty SD female rats (20 week-old) with body weight of 250-280 g were mated with 20 SD male rats with body weight of 250-280 g

and the female rats with vaginal plug of white crystalline particles were determined as pregnant rats. Twelve pregnant rats were divided into diabetic group (n=6) and control group (n=6). On day 0 of gestation

the diabetic group was treated by single intraperitoneal injection of streptozotocin (35 mg/kg)

while the control group was injected with normal saline. Systolic blood pressure (SBP) of the offsprings was monitored by tail-cuff non-invasive continuous blood pressure system. Six 20-week-old offsprings with body weight of 250-280 g were randomly selected from the diabetes group and the control group respectively to detect 24-hour urine flow using stainless steel metabolic cages and urinary sodium excretion with suprarenal artery administration of AT

1

R antagonist candesartan. The renal AT

1

R mRNA levels were measured by qRT-PCR

while the AT

1

R protein levels were detected by Western blotting.       Results      The SBP of the postnatal offsprings from the diabetes group was higher than that from the control group in the 12nd

16th

20th and 24th weeks (118±4 vs 105±3

124±2 vs 114±2

135±3 vs 118±2

and 140±4 vs 120±3 mmHg

respectively

all P0.05). The 24-hour urine analysis showed that the basic urine flow and urinary sodium excretion rate of the offsprings from the diabetes group were significantly lower than those from the control group [558.8±40.5 vs 764.3±87.6 μmol/(kg·d)

P0.05

]

. The candesartan-induced natriuretic and diuretic effect in the offsprings from the diabetes group was stronger than that in the offsprings from the control group (1 560±87 vs 760±60 μL/min

P0.05). Moreover

the renal AT

1

R at mRNA and protein levels in the offsprings from the diabetes group were significantly higher than those in the offsprings from the control group (1.27±0.08 vs 0.57±0.05

and 1.2±0.1 vs 0.5±0.2

P0.05).       Conclusion      Maternal diabetes can induce hypertension in the adult rat offsprings

which may be related with high expression of AT

1

R in kidney and retention of water and sodium.