Information drawn from a number of sources, mainly utilizing electrophysiological and neurochemical techniques, provide compelling evidence that overactivity of the sympathetic nervous system characterizes a substantial proportion of patients with essential hypertension. Nerve firing rates in postganglionic sympathetic fibres in skeletal muscle circulation are increased in hypertensive patients, the degree of activation being directly related to the severity of the hypertensive state. Essential hypertension is also characterized by an increased spillover of the adrenergic neurotrasmitters from the heart and the kidney, thereby participating to a considerable extent at the development and progression of the target organ damage characterizing high blood pressure states. All these neuroadrenergics alterations result to be potentiated when hypertension is associated with obesity, heart failure, renal insufficiency, obstructive sleep apnea, diabetes or metabolic syndrome, making the hypertensive patients particularly exposed to the adverse effects of a sympathetic activation (cardiac arrhythmias, coronary heart disease and sudden death). Although investigated since several years, the mechanisms responsible for the neurogenic abnormalities characterizing hypertension remain largely unknown. Evidence has been provided, however, that alterations in cardiovascular reflex control (baroreceptor, chemoreceptor and/or cardiopulmonary receptor impairment) take place in hypertension, thereby contributing, together with humoral (Angiotensin II) or metabolic (insulin-resistance, leptin, etc.) mechanisms, at enhancing sympathetic cardiovascular drive. This enhancement however appears to be at least in part reversible. This because both non pharmacological (physical training, body weight reduction) and pharmacological (treatment with Ace-inhibitors, Angiotensin II receptor blockers and Central sympatholitic agents) interventions have been shown to exert symapthoinhibitory effects, thereby reducing the overall cardiovascular risk profile of the hypertensive patient.
University of Bristol (2005) J Physiol 567P, SA11
Research Symposium: NEUROADRENERGIC MECHANISMS AND PATHOPHYSIOLOGY OF HYPERTENSION
Grassi, Guido;
1. Clinica Medica, Univ. Milano Bicocca, Milano, Italy.
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Where applicable, experiments conform with Society ethical requirements.