Hypertension Exercise Program

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Hypertension is a major risk factor for the development of atherosclerosis. In hypertensive patients with elevated plasma renin activity, increased incidence of myocar-dial infarction by fivefold has been demonstrated.9 In hypertensive patients, serum concentrations of angiotensin II (Ang-II), an active vasoconstrictor produced by the renin-angiotensin-aldosterone system (RAS), are elevated.10 Ang-II was implicated in acceleration of atherosclerosis11,12 not only by causing hypertension, but also by stimulating proliferation of smooth muscle cells,13 activation of blood platelets,14 and accumulation of cholesterol in arterial macrophages,1517 and by increasing the formation of reactive oxygen species (ROS), such as hydrogen peroxides and other free radicals in plasma18,19 and in macrophages.20 In addition, Ang-II was shown to modify LDL to yield an atherogenic lipoprotein, which is taken up by macrophages at enhanced rate through the scavenger receptors. Ang-II also enhances the uptake of oxidized LDL (Ox-LDL) by macrophages via a proteoglycan-mediated pathway.21 In apolipoprotein E-deficient (E0) mice it was shown that Ang-II type I receptor antagonists and inhibitors of the angiotensin converting enzyme (ACE), which inhibit the production of Ang-II from Ang-I, attenuate the enhanced development and progression of atherosclerosis.22,23 Some of the biological activities of Ang-II were shown to be mediated by aldosterone.24 Experimental evidence suggests that aldos-terone amplifies tissue ACE activity and angiotensin receptor type 1 synthesis.25 Moreover, aldosterone plays an important role in the pathophysiology of heart failure.26 Clinical studies have demonstrated that ACE inhibitors significantly reduce the morbidity and mortality of patients with myocardial infarction or heart failure and reduce the incidence of recurrent myocardial infarction and ischemic events in patients with coronary artery disease, even in the absence of blood pressure lower-ing.27,28 Data from a variety of animal experiments indicate that ACE inhibitors can attenuate the development of atherosclerosis by mechanisms that may be mediated through the prevention of the effect of angiotensin II and also by potentiation of bradykinin formation.29-32

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