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Systemic Hemodynamics in Hypertension

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Hypertension and Cardiovascular Disease
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Abstract

Several lines of research have documented an association between increased sympathetic nervous system activity and hypertension in the young. A widespread autonomic nervous system abnormality, clinically manifested as a hyperkinetic circulation characterized by elevations in heart rate, cardiac output, and plasma norepinephrine levels has been repeatedly demonstrated in the early phases of hypertension [1–6]. The co-distribution of blood pressure and cardiac index was investigated in two large Michigan populations using the mixture analysis method [7]. Distinct subgroups of individuals with elevated blood pressure and cardiac index were identified in both populations, with a prevalence of 17–24 %. Among the subjects in Tecumseh, Michigan, with borderline hypertension (mean age 32 years), 37 % showed a hyperdynamic circulation and other signs of sympathetic overactivity [4]. Sympathetic overactivity may be detected many years before the blood pressure increases to hypertensive levels suggesting that sympathetic activation is a primary event and not a mere consequence of some other aberration [4]. Plasma norepinephrine and epinephrine levels, as well as norepinephrine turnover and platelet norepinephrine content, are elevated in hypertensive subjects [8, 9]. Excessive sympathetic activity in hypertensives has been demonstrated also using spectral analysis of heart rate variability. About 30 % of the young subjects from the Tecumseh Offspring Study had sympathetic predominance at spectral analysis of heart rate variability [10]. In a sample of young adults with stage 1 hypertension from the HARVEST Study, over one third of subjects had sympathetic predominance and reduced heart rate variability [11]. During a 6-year follow-up, subjects with sympathetic predominance developed sustained hypertension requiring antihypertensive treatment three times more frequently than subjects with normal autonomic tone. In addition, at the end of follow-up subjects with sympathetic predominance showed an increase in total cholesterol and body weight and an impairment of large artery compliance. According to some investigators, even normotensive individuals with a positive family history of hypertension may have an increased ratio of sympathetic to parasympathetic activity at the cardiac level [12]. An abnormal autonomic cardiac regulation has been found to be present also in subjects with white-coat hypertension [13, 14]. Fagard et al. found a low-frequency to high-frequency ratio of 1.11 in a group of white-coat hypertensives that was significantly higher than in a group of normotensive subjects of control (0.81) [14]. The impact of enhanced sympathetic activity in hypertension has been confirmed by studies performed with microneurographic assessment of sympathetic nerve traffic to skeletal muscle. A marked increase in muscle sympathetic nervous activity was found in subjects with both borderline and established hypertension [8, 15]. In addition, a number of prospective studies have shown that increased cardiovascular reactivity to stressful stimuli is predictive of future hypertension and that it may contribute to the development of cardiovascular disease [16, 17]. Japanese investigators [18] have shown that increases in baseline plasma norepinephrine are predictive of future blood pressure elevation in normotensive or borderline hypertensive subjects. Julius et al. demonstrated that both sympathetic and parasympathetic blockade were needed to normalize cardiac output in borderline hypertension and that enhanced sympathetic activity was associated with decreased parasympathetic cardiac activity [2]. The above findings strongly suggest that the stimuli for the altered hemodynamic state in the early stage of hypertension emanate from the medulla oblongata, where sympathetic and parasympathetic activities are integrated in a reciprocal fashion. In conclusion, the data from the literature indicate that sympathetic predominance starts early in life and is present in a sizable portion of the hypertensive population. Exaggerated sympathetic activity in hypertension has detrimental effects on target organs and may favor the development of cardiovascular complications. In fact, in addition to its effect on blood pressure, alteration of autonomic nervous system activity may lead to an increase in other cardiovascular risk factors, producing tachycardia, lipid abnormalities, insulin resistance and obesity [19] (Fig. 7.1).

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Palatini, P. (2016). Systemic Hemodynamics in Hypertension. In: Andreadis, E. (eds) Hypertension and Cardiovascular Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-39599-9_7

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  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-39597-5

  • Online ISBN: 978-3-319-39599-9

  • eBook Packages: MedicineMedicine (R0)

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