Sympathetic nervous system activation in essential hypertension, cardiac failure and psychosomatic heart disease

Regional sympathetic activity can be studied in humans using electrophysiol ogical methods measuring sympathetic nerve firing rates and neurochemical t echniques providing quantification of noradrenaline spillover to plasma fro m sympathetic nerves in individual organs. Essential hypertension: Such mea surements in patients with essential hypertension disclose activation of th e sympathetic outflows to skeletal muscle blood vessels, the heart and kidn eys, particularly in younger patients. This sympathetic activation, in addi tion to underpinning the blood pressure elevation, most likely also contrib utes to left ventricular hypertrophy, and to the commonly associated metabo lic abnormalities of insulin resistance and hyperlipidaemia. Antihypertensi ve drugs, such as moxonidine, which act primarily by inhibiting the sympath etic nervous system, should have additional clinical benefits beyond those attributable to blood pressure reduction, in protecting against hypertensiv e complications. Obesity-related hypertension: Understanding the neural pat hophysiology of hypertension in the obese has been difficult. In normotensi ve obesity, renal sympathetic tone is doubled, but cardiac noradrenaline sp illover (a measure of sympathetic activity in the heart) is only 50% of nor mal. In obesity-related hypertension, there is a comparable elevation of re nal noradrenaline spillover, but without suppression of cardiac sympathetic s (cardiac sympathetic activity bring more than double that of normotensive obese and 25% higher than in healthy volunteers). Increased renal sympathe tic activity in obesity may be a 'necessary' cause for the development of h ypertension (and predisposes to hypertension development), but apparently i s not a 'sufficient' cause. The discriminating feature of the obese who dev elop hypertension is the absence of the adaptive suppression of cardiac sym pathetic tone seen in the normotensive obese. Heart failure: In cardiac fai lure, the sympathetic nerves of the heart are preferentially stimulated. No radrenaline release from the failing heart at rest in untreated patients is increased as much as 50-fold, similar to the level seen in the healthy hea rt during near-maximal exercise, Activation of the cardiac sympathetic outf low provides adrenergic support to the failing myocardium, but at a cost of arrhythmia development and progressive myocardial deterioration. Psychosom atic heart disease: No more than 50% of clinical coronary heart disease is explicable in terms of classical cardiac risk factors. There is gathering e vidence that psychological abnormalities, particularly depressive illness, anxiety states, including panic disorder and mental stress, are involved he n,'triggering' clinical cardiovascular events, and possibly also contributi ng to atherosclerosis development. The mechanisms of increased cardiac risk attributable to mental stress and psychiatric illness are not entirely cle ar, but activation of the sympathetic nervous system seems to be of prime i mportance.