Psychogenic hypertension

Abstract

In searching for biological evidence that essential hypertension is caused by chronic mental stress, a disputed proposition, parallels are noted with panic disorder, which provides an explicit clinical model of recurring stress responses: (i) There is clinical comorbidity; panic disorder prevalence is increased threefold in essential hypertension. (ii) Plasma cortisol is elevated in both. (iii) In panic disorder and essential hypertension, but not in health, single sympathetic nerve fibers commonly fire repeatedly within an individual cardiac cycle (these salvoes of nerve firing constituting a stress "signature"). (iv) For both, adrenaline cotransmission is present in sympathetic nerves, as is seen in experimental models of stress. (v) There is induction of the adrenaline synthesizing enzyme, PNMT, in sympathetic nerves, an explicit indicator of mental stress exposure. Patients with essential hypertension exhibit a further manifestation of mental stress: There is activation of noradrenergic brainstem neurons, most likely of the Al and AS nuclei, projecting rostrally to the hypothalamus and amygdala. Activation of the renal sympathetic outflow is pivotal in hypertension development. In the presence of high dietary sodium intake, endemic in contemporary life, this activation of the renal sympathetic nerves provides concurrent "neural," "renal," and "sodium" mechanisms of hypertension development. Relaxation and stress reduction measures lower blood pressure, but less than anticipated, and not sufficient for BP control in severe grades of hypertension. A modern and commonly successful development in the therapeutics of severe and resistant hypertension is the targeting of the final common pathway in the hypertension pathogenesis, with ablation of the renal sympathetic nerves by radiofrequency energy delivered as a one-off procedure, using a specially engineered catheter sited in the renal arteries, the procedure of endovascular renal denervation.