Essential hypertension

Athough a central role of the autonomic nervous system in essential hypertension remains controversial, evidence for a contributory role has been repeatedly documented, particularly in the early hyperkinetic phase of the disease (28). There is also evidence of enhanced norepinephrine spillover in essential hypertension (29) and enhanced sympathetic nerve traffic. However, because many genes that are recently shown to be involved in familial hypertension syndromes have included first and foremost gene products involved in volume regulation in some way, autonomic mechanisms must be viewed as a component rather than the sole player in the pathophysiological mosaic of essential hypertension.

Increased central sympathetic outflow, impaired baroreflex buffering, altered regulation of norepinephrine release, and reuptake can contribute to essential hypertension. The patho-genesis of the sustained or increased central sympathetic drive in essential hypertension is unclear. In the brainstem, noradrenergic neurotransmission inhibits central sympathetic outflow. In contrast, some suprabulbar noradrenergic projections to the hypothalamus and amygdala are sympathoexcitatory. Esler et al. (29,30) estimated norepinephrine turnover from these subcortical suprabulbar brain regions by measuring internal jugular vein overflow of norepinephrine and found it to be increased in patients with essential hypertension. Increased rates of sympathetic nerve firing and a reduction of cardiac neuronal norepinephrine reuptake contribute to essential hypertension. Central noradrenergic turnover correlated with systemic sympathetic activation, suggesting that this mechanism contributes to the sympathetic overactivity that is observed in essential hypertension.

Blood pressure and heart rate are kept within a relatively narrow range appropriate to physiological demands (exercise level or orthostatic stress) by autonomic baroreflex mechanisms. However, substantial variability from heart beat-to-heart beat is present and reflects both the presence of a variety of naturally occurring physiological perturbations to cardiovascular homeostasis and the dynamic response of the cardiovascular control systems to these pertubations (31). Spectral analysis of cardiovascular rhythms has become an important tool in the investigation of autonomic contributions to hypertension. Continuous blood pressure fluctuations are caused by several factors. Respiration modulates blood pressure in the high frequency (HF) band of the breathing rate. Atropine abolishes HF oscillations of heart rate, whereas HF oscillations of systolic blood pressure remain constant. The hypothesis that the vagally mediated HR oscillations associated with respiration generate the respiratory oscillations in blood pressure can therefore be excluded (32). Systolic blood pressure fluctuations with a 10-s periodicity, or low frequency band (LFSBP), which are also termed as "Traube-Hering-Mayer" waves, mainly reflect sympathetic-mediated changes in vasomotor tone (33). Indeed, LFSBP is linked to low frequency oscillations in the activity of postganglionic sympathetic neurons (34). A tight relationship between LFSBP and muscle sympathetic activity could be found in humans (35). LFSBP is increased by maneuvers that induce sympathetic activation, such as upright posture (36,37), lower body negative pressure (38), or infusion of depressor substances (39). LFSBP was similar or increased (40) in hypertensive patients as compared to normotensive subjects.

Ganglionic blockade has been quite valuable in studies that deal with sympathetic outflow in hypertension. Trimethaphan (Afronad) is an adrenergic, anticholinergic, antihypertensive, and ganglionic blocking agent, which for many years was marketed for intravenous therapy of hypertension in the United States. It prevents transmission in both adrenergic and cholinergic ganglia by blocking Nn postganglionic receptors (Fig. 1). It also has a minor direct peripheral arterial and venous vasodilatory effect and is a weak histamine releaser.

The contribution of the sympathetic nervous system in hypertension can be examined by gaging the decrease in blood pressure produced by acute sympathetic withdrawal during ganglionic blockade (15,40,41). Studies with ganglionic blockade reveal that sympathetic nervous system contributes to essential hypertension, and severes supine hypertension in patients with multiple system atrophy (MSA) (40).

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