The autonomic nervous system exerts powerful control over human cardiovascular function through many delicate regulatory mechanisms that modulate blood pressure, heart rate (HR), cardiac output, and contractility in a highly specific and targeted manner (1,2). The arterial and cardiopulmonary reflex mechanisms converging on the brainstem (3,4) are perhaps the best studied systems, but others such as cortical, insular cortical, and amygdala centers, and renal and skeletal muscle afferents have important effects as well. Visceral sympathetic afferent reflexes may also contribute to pressor mechanisms (5).
in contrast to the well-appreciated role of the autonomic nervous system in the minute-by-minute regulation of these variables, the role of the sympathetic nervous system in producing chronic hypertension has remained controversial over many decades. certainly there is little doubt that the sympathetic nervous system plays a contributory role in most hypertension, as evidenced by baroreflex resetting, but in some cases, here
From: Contemporary Endocrinology: Hypertension and Hormone Mechanisms Edited by: R. M. Carey © Humana Press Inc., Totowa, NJ
Some Presentations of Neurogenic Human Hypertension
Medullary vascular compression
Severe paroxysmal hypertension
Supine hypertension of autonomic failure
Postural tachycardia syndrome collectively termed as neurogenic hypertension, it seems to be the primary signal eliciting the effect.
Although there are many causes of neurogenic hypertension, the following are the best established and most widely studied entities proposed to be related to sympathetic mechanisms to date (Table 1): baroreflex failure, medullary vascular compression, severe paroxysmal hypertension, alcohol withdrawal, essential hypertension, obesity, sleep apnea, and postural tachycardia syndrome (POTS).
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