Nitrates and Arterial Function
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HYPERTENSION (M SAFAR, SECTION EDITOR)
Nitrates and Arterial Function Wilmer W. Nichols & Krishna Harripersaud & John W. Petersen
Published online: 2 April 2013 # Springer Science+Business Media New York 2013
Abstract In this article we trace the history of nitrites and nitrates from their discovery to their widespread use in clinical medicine. The cardiovascular actions and uses of these molecules [namely endogenous nitric oxide (NO) and exogenous nitroglycerin (NTG)] are described along with their similar mechanisms of action. The major vasodilating effect of both NO and NTG is on muscular arteries with less effect on arterioles and veins. By decreasing arterial stiffness, these agents reduce pulse wave velocity (PWV) and attenuate wave reflection amplitude and duration. These alterations in arterial properties and wave reflection characteristics reduce pulsatile left ventricular (LV) afterload (systolic and pulse blood pressure) and LV wasted energy, which decrease myocardial oxygen requirements. These agents can also increase arteriolar and venous caliber, which decreases distal resistance and increases venous capacity, respectively. These mechanistic effects help to explain the benefit of nitrites and nitrates in control of angina pectoris, congestive heart failure, and systolic hypertension. Keywords Nitrates . Nitrites . Wave reflection . Wasted left ventricular energy . Myocardial oxygen demand . Endothelial function . Arterial function . Arterial stiffness . Pulse wave velocity
W. W. Nichols (*) : K. Harripersaud : J. W. Petersen Division of Cardiovascular Medicine, Department of Medicine, University of Florida College of Medicine, Box 100277, Gainesville, FL 32610, USA e-mail: [email protected] K. Harripersaud e-mail: [email protected] J. W. Petersen e-mail: [email protected]
Introduction Arterial properties and wave reflection characteristics are independent predictors of adverse cardiovascular events, including mortality [1, 2]. As arteries become stiffer (eg, with age, hypertension, diabetes, etc) measured central aortic systolic and pulse pressures are augmented [3]. The aortic pressure wave is determined by the interaction (or algebraic sum) of a LV ejected forward traveling “incident” wave and a later arriving backward traveling reflected wave from the lower body [1–9]. Characteristics of the forward traveling wave depend, primarily, upon the elastic properties of the ascending aorta and are not influenced by wave reflections [3, 10, 11]. Two visible demarcations usually occur on the initial upstroke of the central aortic pressure wave in individuals with a stiff aorta and/or peripheral vasoconstriction; the first shoulder (Pi – Pd) and the inflection point, Pi (see Fig. 1 below). The first (or early) shoulder (or percussion wave) is generated by LV ejection and occurs at peak blood flow velocity while the inflection point occurs later and denotes the initial upstroke of the reflected pressure wave (Ps – Pi); this wave represents the second (or mid-to-late) systolic shoulder
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