Nitric oxide interacts with the renin-angiotensin system to control vascular tension and systemic arterial circulation in renal hypertensive rats.
Aortic findings in renal hypertensive rats should not change practice; leaves open NO-RAAS interactions in human hypertension.
We investigated the interaction between nitric oxide and the renin angiotensin system in regulating isolated aortic tension and mean arterial pressure in renal hypertensive rats (RHR). Acetylcholine (ACh) relaxed aorta precontracted with norepinephrine from RHR significantly less than that from nor-motensive rats (NR) (Emax: 34.3% and 86.0%, respectively, P<0.01). The ACh-induced relaxation was significantly enhanced by losarían (P < 0.05) and completely abolished by removal of endothelium or NG-nitro-L-arginine methyl ester (L-NAME). ACh lowered the mean arterial pressure slightly less effectively in RHR than in NR (6.8 and 13.0 mmHg, respectively, at 0.1 μg/kg), whereas the depressor effect was reduced by L-NAME (—15.5 and 10.3 mmHg, respectively, at 0.1 μg/kg), but rather enhanced by further treatment with losarían (9.9 (P<0.05) and 17.3 mmHg, respectively, at 0.1 μg/kg). Angiotensin II induced similar contractile and pressor responses in both RHR and NR, and these effects were significantly enhanced by L-NAME, except for the pressor effect in RHR. L-NAME induced a similar pressor response in RHR and NR (15.9 and 15.2 mmHg, respectively, at 0.1 mg/kg), the effect being decreased by pretreatment with losartan. Losartan induced a depressor response thai was smaller in RHR ihan in NR (34.0 and 48.8 mmHg, respectively, ai 0.3 mg/kg), and Ihe response was significanily reduced by L-NAME. These results suggest that nitric oxide interacts with the renin angiotensin system to control the vascular tension and systemic arterial circulation in RHR.
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Lee et al. (1997) studied this question.
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