J Török1, F Kristek. 1. Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, Bratislava, Slovak Republic.
Abstract
OBJECTIVES: To determine the reactivity and accompanying structural changes in thoracic aorta and carotid artery from nitric oxide (NO)-deficient hypertensive and spontaneously hypertensive rats (SHR). ANIMALS AND METHODS: For the functional study, isolated rat arterial rings were precontracted with a submaximal concentration of phenylephrine (1 muM) and relaxant responses to cumulative concentrations of acetylcholine were obtained. For the morphological study, arteries were processed by a standard method for electron microscopy. The geometry of the arteries - the inner diameter and the wall thickness (tunica intima plus tunica media) - was evaluated by light microscopy. RESULTS: Increased systolic blood pressure was accompanied by increased heart weight to body weight ratio in both NO-deficient and SHR compared with normotensive controls, indicating cardiac hypertrophy. Morphometry of the thoracic aorta and carotid artery in both models of hypertension showed increased wall thickness, cross-sectional area and wall to diameter ratio. The inner diameter increased in aorta but not in carotid artery. In isolated arteries from normotensive rats, the addition of acetylcholine to precontracted vessels resulted in dose-dependent relaxation. The relaxing effect was more prominent in thoracic aorta than in carotid artery. Endothelium-dependent relaxation of arteries from NO-deficient hypertensive rats was markedly reduced. On the other hand, in aorta and carotid artery from SHR, the endothelium-dependent relaxation in response to acetylcholine was not significantly attenuated. The relaxation of arteries from SHRs, as well as the residual relaxation of arteries from NO-deficient hypertensive rats, was abolished by addition of N(G)-nitro-l-arginine methyl ester, an inhibitor of NO synthase, to the incubation medium. CONCLUSIONS: These results suggest that increased systolic blood pressure and accompanying structural changes are not primarily responsible for impairment of endothelium-dependent relaxation in experimental hypertension.
OBJECTIVES: To determine the reactivity and accompanying structural changes in thoracic aorta and carotid artery from nitric oxide (NO)-deficient hypertensive and spontaneously hypertensiverats (SHR). ANIMALS AND METHODS: For the functional study, isolated rat arterial rings were precontracted with a submaximal concentration of phenylephrine (1 muM) and relaxant responses to cumulative concentrations of acetylcholine were obtained. For the morphological study, arteries were processed by a standard method for electron microscopy. The geometry of the arteries - the inner diameter and the wall thickness (tunica intima plus tunica media) - was evaluated by light microscopy. RESULTS: Increased systolic blood pressure was accompanied by increased heart weight to body weight ratio in both NO-deficient and SHR compared with normotensive controls, indicating cardiac hypertrophy. Morphometry of the thoracic aorta and carotid artery in both models of hypertension showed increased wall thickness, cross-sectional area and wall to diameter ratio. The inner diameter increased in aorta but not in carotid artery. In isolated arteries from normotensive rats, the addition of acetylcholine to precontracted vessels resulted in dose-dependent relaxation. The relaxing effect was more prominent in thoracic aorta than in carotid artery. Endothelium-dependent relaxation of arteries from NO-deficient hypertensiverats was markedly reduced. On the other hand, in aorta and carotid artery from SHR, the endothelium-dependent relaxation in response to acetylcholine was not significantly attenuated. The relaxation of arteries from SHRs, as well as the residual relaxation of arteries from NO-deficient hypertensiverats, was abolished by addition of N(G)-nitro-l-arginine methyl ester, an inhibitor of NO synthase, to the incubation medium. CONCLUSIONS: These results suggest that increased systolic blood pressure and accompanying structural changes are not primarily responsible for impairment of endothelium-dependent relaxation in experimental hypertension.