Pp. 241-280 (40)
Gonul Simsek and Aykut Oruc
In this section, we discuss the cardiovascular pathways of the central
nervous system (CNS), neural regulation of circulation and patophysiologic
mechanisms of neurogenic hypertension. The pathophysiologic mechanisms underlying
the increased arterial pressure in neurogenic hypertension are not clear. It has been
suggested that sympathetic overactivity is present in hypertensive patients. The role of
sympathetic outflow in the pathogenesis of hypertension has been an issue of
continuous interest recently. Why sympathetic activity rises in neurogenic hypertension
is unclear. In this section, proposed causes of increased sympathetic tone in essential
hypertension; especially the factors causing impaired baroreflex sensitivity (i.e.
aldosterone and locally produced chemical factors such as prostacyclin, prostaglandins,
nitric oxide (NO), reactive oxygen species (ROS) and platelet factors),direct effects of
NO, ROS, angiotensin II, salt and proinflammatuar cytokines to CNS factors that play
role on impaired sympathetic activity in aging and obesity processes (i.e. leptin,
insulin, insulin resistance, adiponectin and ghrelin) are discussed.
Adiponectin, Aging, Angiotensin II, Baroreceptor sensitivity, Blood
pressure, Chemoreceptors, Dietary salt, Ghrelin, Inflammation, Insulin resistance,
Insülin, Leptin, Neurogenic hypertension, Nitric oxide, Obesity, Oxidative stress,
Prostacyclin, Prostaglandins, Sympathetic activity, Vasopressin.
Department of Physiology, Istanbul University-Cerrahpaşa, Cerrahpasa Faculty of Medicine Istanbul, Turkey.