Bibliography - Sympathetic Nervous System

Advances in the role of the Sympathetic Nervous System in cardiovascular medicine

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The sympathetic neurobiology of essential hypertension: disparate influences of obesity, stress and noradrenaline transporter dysfunction?

M. Esler, M. Rumantir, D. Kaye, G. Lambert.

Summary

Although the importance of sympathetic nervous activation in the pathogenesis of essential hypertension is well documented, the exact pathophysiology of the sympathetic nervous dysfunction present remains to be delineated. This review details three relatively new findings of disturbed sympathetic neurobiology in hypertension.
Adrenaline cotransmission is present in the cardiac sympathetic nerves of patients with essential hypertension, as it is in patients with panic disorder, providing presumptive evidence of exposure to high levels of mental stress in hypertensive patients. In lean patients with hypertension there is also evidence of faulty noradrenaline reuptake into the sympathetic nerves of the heart, an abnormality amplifying the sympathetic neural signal by impairing removal of noradrenaline from the synaptic cleft. If both abnormalities are present in the sympathetic nerves of the kidneys also (which we did not test), there would most probably be a direct contribution to hypertension development. In the kidneys the causal chain between sympathetic overactivity and the development of hypertension is stronger than for the heart. In obesity-related hypertension there is evidence that renal sympathetic tone is high, based on approximately a doubling of the measured rate of spillover of noradrenaline into the renal veins. This increase in sympathetic outflow to the kidneys appears to be a necessary but apparently not a sufficient cause for the development of clinical hypertension, commonly being present also in overweight people with blood pressure in the normotensive range. High renal sympathetic tone in the latter, of course, may well still contribute to elevation of their pressure level, although not on such a scale as to cause clinical hypertension.

Am J Hypertens. 2001;14:139S-146S.

Commentary

After a short introduction on the measurement of sympathetic nervous function in human hypertension (by means of microneurography and noradrenaline spillover) the authors discuss in detail the sympathetic neurobiology in essential hypertension.

New findings in this field are the following:

1/ In patients with essential hypertension adrenaline cotransmission occurs in the cardiac nerves.This situation resembles conditions of panic disorders, providing presumptive evidence of exposure to high levels of mental stress in hypertensive patients.

2/ In lean hypertensive patients noradrenaline reuptake by the cardiac sympathetic nerve endings appears to be reduced, thus leading to an increased level of noradrenaline within the synaptic cleft.

3/ In obese hypertensives (who are numerous) renal sympathetic tone is high, as reflected by an increased rate of spillover into renal veins. This process is also observed in obese persons with normal blood pressure.

These newer experimental findings confirm the potential beneficial activities of various antiadrenergic therapies of hypertensive disease. Accordingly, centrally acting agents appear to owe their beneficial effects to antiadrenergic activities. The same holds for nonpharmacological measures such as dietary calorie restriction and the stimulation of exercise, which are known to suppress sympathetic nervous system activity in the long term.