Vascular Compression of the Rostral Ventrolateral Medulla in Sympathetic Mediated Essential Hypertension (original) (raw)

Essential hypertension as a result of neurochemical changes at the rostral ventrolateral medulla

2013

Acute ischemia of the brainstem has been known to produce hypertension. After an initial review of central nervous system mechanisms contributing to systemic hypertension and the impact of the rostral ventrolateral medulla (RVLM) on arterial pressure, the authors propose that essential hypertension involves neurochemical changes at the level of the RVLM which are triggered by cerebral ischemia. Experimental and clinical data are presented to show that there is a link between ischemia of the brainstem and chronic hypertension. Atherosclerosis of the cerebral circulation leads to ischemia of the RVLM and other regions with autonomic function. This ischemic process results in increased availability of angiotensin II in the RVLM, which maintains the chronic hypertensive state via either direct stimulation of the RVLM or exacerbation of brainstem ischemia due to increased vasoconstriction.

Arterial hypertension and neurovascular compression at the ventrolateral medulla

Journal of Neurosurgery, 1992

✓ Intraoperative observations and animal experiments suggest that neurovascular compression at the left ventrolateral medulla is a possible etiological factor in essential hypertension. In pursuing this hypothesis, the authors examined the neurovascular relations in the posterior cranial fossa of 24 patients with essential hypertension, of 10 with renal hypertension, and of 21 normotensive control patients. Artificial perfusion of the vessels and microsurgical investigations during autopsy identified the vascular relations at the brain stem and at the root entry zone of the caudal cranial nerves. There was no evidence of neurovascular compression at the ventrolateral medulla on the left side in any patient from the control group or among those with renal hypertension. Two normotensive patients had neurovascular compression at the right ventrolateral medulla by the posterior inferior cerebellar artery. In contrast, all patients with essential hypertension had definite neurovascular c...

Role of the Medulla Oblongata in Hypertension

Hypertension, 2001

Brain pathways controlling arterial pressure are distributed throughout the neuraxis and are organized in topographically selective networks. In this brief review, we will focus on the medulla oblongata. The nucleus tractus solitarius (NTS) is the primary site of cardiorespiratory reflex integration. It is well accepted that lesions or other perturbations in the NTS can result in elevations of arterial pressure (AP), with many of the associated features so commonly found in humans. However, recent studies have shown 2 distinct subpopulations of neurons within the NTS that can influence AP in opposite ways. Commissural NTS neurons located on the midline may contribute to maintenance of hypertension in spontaneously hypertensive rats (SHR), because small lesions in this area result in a very significant reduction in AP. Also involved in this blood pressure regulation network are 2 distinct regions of the ventrolateral medulla: caudal (CVLM) and rostral (RVLM). Neurons in CVLM are thought to receive baroreceptor input and to relay rostrally to control the activity of the RVLM. Projections from CVLM to RVLM are inhibitory, and a lack of their activity may contribute to development of hypertension. The RVLM is critical to the tonic and reflexive regulation of AP. In different experimental models of hypertension, RVLM neurons receive significantly more excitatory inputs. This results in enhanced sympathetic neuronal activity, which is essential for the development and maintenance of the hypertension. (Hypertension. 2001;38[part 2]:549-554.

Neurovascular compression: sympathetic activity in severe arterial hypertension

Physiological research / Academia Scientiarum Bohemoslovaca, 2009

Compression of the rostral ventrolateral medulla oblongata (RVLM) by an abnormally located artery is regarded as one possible cause of arterial hypertension. There exists a limited set of data suggesting that increased sympathetic activity in patients with RVLM compression may lead to arterial hypertension. Accordingly, we decided to assess the sympathetic activity in patients with severe arterial hypertension and to investigate any correlation with the presence of RVLM compression. Sixty-four patients with severe arterial hypertension were enrolled in our study. Sympathetic activity was evaluated using 24-hour urinary norepinephrine as measured by high-pressure liquid chromatography with electrochemical detection. The presence of RVLM compression was assessed with magnetic resonance imaging. Neurovascular compression of the RVLM was identified in 40 patients, 27 of whom presented left-sided compression. Twenty-four hour urinary norepinephrine averaged 263.6+/-135.9 nmol in patients...

Neurovascular compression and essential hypertension

Neuroradiology, 1991

The pathogenesis of essential hypertension still remains unclear. Recently, it has been supposed, that an arterial compression of the left root entry zone (REZ) of the cranial nerves IX and X by looping arteries may play a pathogenetic role. In this report we verified this hypothesis retrospectively by vertebral angiographies in 99 hypertensive and 57 normotensive patients. The angiographic findings were compared with the results obtained from an anatomic study, in which the positions of 10 left vagus/glossopharyngeal nerves in the skull were radiographically determined in 10 cadavers. By using a pattern of REZ topography developed from this information we obtained the following results: In 81% of the evaluable angiographies of hypertensive patients we found an artery in the left REZ of cranial nerves IX and X. The normotensive patients showed an artery in the REZ only in 41.7% of cases. Our results support the hypothesis that essential hypertension may be combined with neurovascular compression of the left REZ of cranial nerves IX/X.

Neural mechanisms in hypertension and the elderly

Archives of Gerontology and Geriatrics, 1995

Experimental animal studies carried out over the past 40 years have unequivocally shown that neurogenic mechanisms are involved in the pathogenesis of hypertension. The results of these studies also suggest that neural factors are important not only in the development but also in the maintenance of the high blood pressure condition. Whether this is the case also for human hypertension has been matter of debate for several decades. However, recent studies in man by employing sophisticated techniques for assessing sympathetic tone, i.e. the norepinephrine radiolabelled technique and microneurographic recording of sympathetic nerve traffic, support the hypothesis that alterations in sympathetic modulation of the cardiovascular system take place in hypertension and may have a pathogenetic relevance in agerelated blood pressure increase.