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Neurovascular abnormalities in the pathogenesis of primary (essential) hypertension

Norman M Kaplan, MD
Section Editor
George L Bakris, MD
Deputy Editor
John P Forman, MD, MSc


The pathogenesis of primary hypertension (formerly called "essential" hypertension) remains incompletely understood. It is generally felt that different factors may contribute in an individual patient. Among the factors that have been intensively studied and that are reviewed separately are salt intake, obesity and insulin resistance, the renin-angiotensin system, and the sympathetic nervous system. In the past few years, a number of other factors have been evaluated, including genetics, endothelial dysfunction, low birth weight, and neurovascular anomalies [1].

The possible role of a specific neurovascular abnormality, compression of the left lateral medulla, in the pathogenesis of primary hypertension is presented in this topic review. Other central and peripheral sympathetic nervous system abnormalities are almost certainly involved in the pathogenesis of primary hypertension.


Experimentally, lesions of the nucleus tractus solitaire in the medulla produce a labile form of hypertension in rats. Clinically, manifestations of sympathetic nervous system hyperfunction may be seen in "hyperkinetic" hypertensives [2,3].

An intriguing connection between the experimental and clinical evidence has been claimed by Dr. Peter Jannetta, a neurosurgeon at the University of Pittsburgh School of Medicine. In 1966, he began performing "microvascular decompression" (MVD) of one or another cranial nerves at the lateral aspect of the medulla by placing a plastic implant between the nerve and blood vessels which were thought to be compressing the nerve and thereby giving rise to hemifacial spasm, trigeminal neuralgia, tinnitus or various other cranial nerve problems [4]. In the course of over 1000 MVDs, compression of the left lateral medulla by looping arteries was noted in 53 hypertensive patients having the procedure for unrelated cranial nerve dysfunction. Vascular decompression of the medulla was performed in 42 of these patients, 32 of whom had relief from hypertension. The duration of follow-up was not provided. Subsequently, Jannetta and colleagues produced hypertension in baboons by connecting a balloon placed at the ventrolateral medulla to another balloon in the thoracic aorta, producing continuous pulsatile compression of the medulla [5].

Apparent confirmation of this connection came from two subsequent studies. In the first, neurovascular compression of the left ventrolateral medulla was found at autopsy in 24 of 24 patients with primary hypertension (formerly called "essential" hypertension) but in none of 10 renal hypertensives or 21 normotensives [6]. In the second report, the vessels in this area were evaluated by T2-weighted imaging and magnetic resonance angiography [7]. Evidence of left-sided vascular compression of the ventrolateral medulla was seen in 20 of 24 patients with primary hypertension as compared to only two of 12 with renal parenchymal hypertension and one of 14 normotensive subjects.


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Literature review current through: Sep 2016. | This topic last updated: Apr 27, 2015.
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