Angiotensin II, but not norepinephrine, potentiates glucose induced hypertension in rats

Angiotensin II (AngII) is unique among pressor hormones in its interactive association with insulin sensitivity. This study tested the hypothesis that chronic AngII hypertension would amplify glucose-induced hypertension greater than would chronic norepinephine (NE) infusion. Male Sprague-Dawley rats were divided into 3 groups: i) Control(C) Glucose (n=6), ii) NE-Glucose (n=3) and iii) AngII-Glucose (n=6). AngII (5ng/kg/min), NE (5ng/kg/min), or vehicle was infused iv. for 5 days, and mean arterial pressure (MAP;18h/d) averaged 88±3, 112±3, and 110±4mmHg, respectively. A 12-day glucose infusion (18.8 mg/day, iv.) increased MAP to 99±3 mm Hg in the C group, similar to our previous reports, while MAP in the NE and AngII groups averaged 126±6 and 140±9 mmHg. The change in MAP caused by glucose was approximately11, 14, and 30 mmHg for the C, NE, and AngII groups. GFR during the control period averaged 2.4±0.2, 2.1±0.2, and 2.6±0.2 ml/min in C, NE, and AngII groups, respectively, and 3.1±0.7, 2.3±0.4, and 1.6±0.2 ml/min on day 4 of glucose infusion. Thus, hypertension caused by chronic glucose infusion in rats was potentiated significantly by modest AngII hypertension, and the response in the NE rats suggests that there is an effect of AngII over and above the effect of hypertension per se. The significant difference in GFR suggests a renal mechanism may be involved.

(Supported by HL 56259 and HL 75625.)