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Book ChapterDOI

Left Ventricular Hypertrophy and Sympathetic Activity

TLDR
Pressure and/or volume overload has been regarded in the past as the leading mechanism through which an increase in blood pressure may trigger the development of left ventricular hypertrophy, but studies performed in recent years have suggested that not only mechanical but also sympathetic, genetic and hormonal factors may significantly contribute to the developed of the cardiac structural alterations.
Abstract
Pressure and/or volume overload has been regarded in the past as the leading mechanism through which an increase in blood pressure may trigger the development of left ventricular hypertrophy1. However, studies performed in recent years both in experimental animals and in man have suggested that not only mechanical but also sympathetic, genetic and hormonal factors (e.g. angiotensin II, insulin, thyroid hormones, etc) may significantly contribute to the development of the cardiac structural alterations frequently detected in the clinical course of the hypertensive state2,3.

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Citations
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Journal ArticleDOI

Metabolic Syndrome in the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) Study: Daily Life Blood Pressure, Cardiac Damage, and Prognosis

TL;DR: The prevalence of metabolic syndrome and its relationship with daily life blood pressure, cardiac damage, and prognosis were determined in 2013 subjects from a Northern Italian population aged 25 to 74 years as discussed by the authors.
Journal ArticleDOI

Sympathetic neural activity in hypertension and related diseases.

TL;DR: Evidence is provided that sympathetic activation represents a hallmark of the essential hypertensive state and the rationale for the use of antihypertensive and cardiovascular drugs capable to exert sympatho-inhibitory effects is represented.
Journal ArticleDOI

Role of the Sympathetic Nervous System in Hypertension and Hypertension-Related Cardiovascular Disease

TL;DR: The paper will finally review the pharmacological and non-pharmacological interventions acting on the sympathetic drive and emphasis will be given to the new approaches, such as renal nerves ablation and carotid baroreceptor stimulation, which have been shown to exert sympathoinhibitory effects.
Journal ArticleDOI

Regression of left ventricular mass with captopril and metoprolol, and the effects on glucose and lipid metabolism.

TL;DR: Angiotensin II and insulin have been suggested to promote the development of hypertensive left ventricular (LV) hypertrophy and the effects of captopril and metoprolol on the regression of LV mass and the relation to insulin sensitivity are compared.
Journal ArticleDOI

Relationship of clinic, ambulatory, and laboratory stress blood pressure to left ventricular mass in overweight men and women with high blood pressure.

TL;DR: It is suggested that cardiovascular responses to behavioral stress are associated with individual differences in LVMI in men and women with high blood pressure who are overweight.
References
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Journal ArticleDOI

Elevated sympathetic nerve activity in borderline hypertensive humans. Evidence from direct intraneural recordings.

TL;DR: The hypothesis of elevated central sympathetic neural outflow in borderline hypertension is supported and plasma norepinephrine levels in the borderline hypertensive group tended to be higher on low sodium diet and lower on high sodium diet.
Journal ArticleDOI

Plasma catecholamines and essential hypertension. An analytical review.

David S. Goldstein
- 01 Jan 1983 - 
TL;DR: The preponderance of literature on the subject supports the hypothesis that increased plasma catecholamine concentrations occur in some patients with essential hypertension, and is consistent with a pathophysiologic role for increased sympathetic neural activity in this subgroup of hypertensive patients.
Journal ArticleDOI

Cardiac Hypertrophy in Spontaneously Hypertensive Rats

TL;DR: The changes in ventricular weight with the onset of hypertension and with its reversal or its prevention suggest that blood pressure might not be the sole factor contributing to cardiac hypertrophy in the spontaneously hypertensive rat and that the renin-angiotensin system might play a permissive role enhancing myocardialhypertrophy.
Journal ArticleDOI

Determination of norepinephrine apparent release rate and clearance in humans.

TL;DR: The findings suggest that methods which measure the dynamic processes of norepinephrine release and removal quantify sympathetic nervous activity better than steady state plasma norpinephrine measurements alone.
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