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OBJECTIVE: This study aimed to evaluate the levels of the adipokines, resistin and adiponectin in normotensive and high normal blood pressure patients. METHODS: Circulating levels of the adipokines, resistin and adiponectin were measured by enzyme-linked immunosorbent assay (ELISA; R'D Systems, Minneapolis) in 20 high normal blood pressure patients and in 20 age-matched normotensive non-diabetic subjects. Statistical analysis was performed with analysis of variance (ANOVA). RESULTS: The control group showed non-significantly decreased levels of resistin when compared with patients with high normal blood pressure [systolic 130-139 mmHg; diastolic 85-89 mmHg] (12.25 vs 14.38 pg/mL, p = 0.40). There were significantly higher levels of adiponectin in the control group when compared with high normal blood pressure patients (11.3 vs 7.51 µg/mL, p = 0.028). CONCLUSIONS: High normal blood pressure patients have increased levels of resistin and lower values of adiponectin when compared with age-matched non-diabetic normotensive subjects. This may explain why those patients showed more progression to hypertension, atherosclerosis and cardiovascular risk than normotensive subjects.

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It has been suggested that the low incidence of cardiovascular diseases in premenopausal women, compared with that in men of the same age, is related to the interaction between the nitric oxide (NO) pathway and estrogens. The aim of the present work was to characterize the mechanism by which 17-beta estradiol produces an increment in NO release in cultured endothelial cells. Treatment of cells with 17-beta estradiol significantly increased the amount of nitrites delivered into the culture medium, compared with that from cells without estrogenic treatment. This effect was blocked by the antagonist of estrogen receptors, tamoxifen. By Western blot, it was shown that 17-beta estradiol significantly increased the amount of eNOS in treated cells, compared with that from their respective control cells. Moreover, the acetylcholine-induced release of nitrites in cells treated with 17-beta estradiol was higher than nitrite production induced by the same dose of acetylcholine in control cells. In conclusion, our data underline the physiological role of 17-beta estradiol, which promotes the increase in eNOS expression, potentiating the effects of vascular agonists that release nitric oxide, suggesting a cardiovascular protective role by estrogens.

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It has been suggested that angiotensin II can be synthesized by other enzymatic pathways besides angiotensin converting enzyme. We evaluated the importance of angiotensin converting enzyme in the coronary circulation during the development of hypertension. Hearts obtained from normotensive (n = 4) and hypertensive rats (n = 4) as well as from hypertensive rats treated with ramipril (n = 4) were stimulated with either angiotensin II or angiotensin I. In a Langendorff perfusion system, angiotensin II induced a greater dose-dependent coronary vasoconstriction in the hearts of hypertensive rats than in normotensive rats (p < 0.05). Furthermore, angiotensin I also induced coronary vasoconstriction, which was greater in the hearts of hypertensive rats than in normotensive rats (p < 0.05). Acute angiotensin converting enzyme inhibition reduced angiotensin I-induced vasoconstriction by 78% in the hearts of normotensive rats and by 82% in the hypertensive rats (p < 0.05), whereas in vivo angiotensin converting enzyme inhibition potentiated angiotensin I-induced vasoconstriction in the hearts of normotensive and hipertensive rats (p < 0.05). Bradykinin receptor's blockade decreased ramiprilat's inhibitory effect on angiotensin I-induced vasoconstriction (p < 0.05). Thus, the present study suggests that, in coronary circulation, angiotensin II synthesis is mainly angiotensin converting enzyme dependent. However, chronic in vivo inhibition could favor induction of other enzymes involved in angiotensin II synthesis. Evenmore, it is possible that the effect of angiotensin converting enzyme inhibition in coronary circulation depends on bradykinin activity.

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Nitric oxide is an important regulator of vascular tone. Deficiencies in nitric oxide release have been implicated in hypertension. In the present study we evaluated vascular reactivity to phenylephrine and acetylcholine in isolated aorta ring preparations from sham and aortic coarctation-induced hypertensive rats and nitric oxide release under resting conditions and after stimulation with acetylcholine. Aortic vessels were divided in upper segment and lower segment in relation to the coarctation; both segments were tested for vascular reactivity and nitric oxide release. Phenylephrine produced higher vasoconstriction in upper segments from hypertensive rats compared to sham operated animals. Lower segments in both experimental groups were not significantly different. Relaxation produced by acetylcholine showed a higher EC50 in the upper segments from hypertensive rats; lower segments in both experimental groups were not significantly different. Aortic rings from hypertensive rats had a higher level of nitric oxide release compared to sham operated rats. Lower segments from hypertensive rats released significantly more nitric oxide. These results suggest that shear stress induced nitric oxide release in lower aortic segments from aortic coarctation-induced hypertensive rats.

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Vasorelaxant activity induced by nitric oxide has been associated with a regulator activity on the blood pressure. In the present study we evaluated the nitric oxide contribution of the regulation of angiotensin II-induced vasoconstriction in normotensive rats and aortic coarctation-induced hypertensive rats. Renal vascular reactivity to angiotensin II was evaluated in the presence and absence of nitric oxide synthesis inhibitor; NG-nitro-L-arginine methyl ester. Nitrite concentration in perfusate was measured as an index of nitric oxide released and nitric oxide synthase activity was determined by production of 3H-L-citrulline. Renal NG-nitro-L-arginine methyl ester perfusion potentiated angiotensin II-induced vasoconstriction in normotensive rats but did not affect angiotensin II effect on hypertensive rats. The release of nitrites was lower in the kidneys from hypertensive rats than normotensive rats. Renal nitric oxide synthase activity was decreased in the hypertensive rats compared to the normotensive rats. We suggest that in normotensive rats, nitric oxide counteracts angiotensin II vasoconstrictor action, whereas, in hypertensive rats this mechanism is impaired, therefore, potentiating angiotensin II increase in vascular resistance thereby contributing to the developing of high blood pressure.

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Independently of it's effects on the coagulation cascade, thrombin can interact with the endothelium and release vasodilatory mediators as prostacyclin, endothelium dependent relaxing factor and potentiate the vascular changes induced by vasoconstrictors like endothelin or cathecolamines. Therefore, in the present study we tested the effect of thrombin in the pulmonary and femoral canine arteries and compared it with the effects on human umbilical artery; we also explore the possible mechanism of action of thrombin-induced changes in vascular tone by using specific inhibitors. Thrombin induced a concentration-dependent and endothelium-dependent relaxation on canine arteries (pulmonary or femoral) and endothelium-independent contraction of human umbilical arteries, neither the relaxation nor the contraction were significantly affected by incubation of the vessels with: a cyclooxygenase inhibitor (indomethacin), lypooxygenase inhibitor (BW 755C) or a soup of antagonists (atropine, metysergyde, propanolol, meperamine or phenoribenzamine) to block muscarinic, histaminic, serotoninergic or adrenergic receptors. However, incubation of the vessels with heparin or a calcium channel blocker did prevented the vasoconstrictor effect of thrombin in human umbilical veins. This results suggests that thrombin can elicit changes in vascular tone and the effect is dependent of the vessel stimulated, and the presence of the endothelium. Thus, thrombin-dependent change in vascular tone is not mediated by arachidonic acid metabolites, sympathetic or parasympathetic neurotransmitters, histamine or serotonine receptors. Thrombin effects may be mediated by interaction with an specific receptor coupled with a calcium signal.

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