Neurogenic hypertension and elevated vertebrobasilar arterial resistance: is there a causative link?

Torbay Hospital, Lawes Bridge, Torquay, TQ2 7AA, UK.
Current Hypertension Reports (Impact Factor: 3.9). 05/2012; 14(3):261-9. DOI: 10.1007/s11906-012-0267-6
Source: PubMed

ABSTRACT There is evidence of sympathetic overdrive in a significant proportion of patients with essential hypertension and an animal model of the condition, the spontaneously hypertensive rat (SHR). The reasons for this remain elusive. However, there is also evidence of narrowing of the arteries supplying the brainstem in the SHR and hypertensive humans. In this review, we discuss the possible role of brainstem hypoperfusion in driving increased sympathetic activity and hypertension.

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    ABSTRACT: The C1 neurons reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM, IVLM). They use glutamate as a fast transmitter and synthesize catecholamines plus various neuropeptides. These neurons regulate the hypothalamic pituitary axis via direct projections to the paraventricular nucleus and regulate the autonomic nervous system via projections to sympathetic and parasympathetic preganglionic neurons. The presympathetic C1 cells, located in the RVLM, are probably organized in a roughly viscerotopic manner and most of them regulate the circulation. C1 cells are variously activated by hypoglycemia, infection or inflammation, hypoxia, nociception and hypotension and contribute to most glucoprivic responses. C1 cells also stimulate breathing and activate brainstem noradrenergic neurons including the locus coeruleus. Based on the various effects attributed to the C1 cells, their axonal projections and what is currently known of their synaptic inputs, subsets of C1 cells appear to be differentially recruited by pain, hypoxia, infection/ inflammation, hemorrhage and hypoglycemia to produce a repertoire of stereotyped autonomic, metabolic and neuroendocrine responses that help the organism survive physical injury and its associated cohort of acute infection, hypoxia, hypotension and blood loss. C1 cells may also contribute to glucose and cardiovascular homeostasis in the absence of such physical stresses and C1 cell hyperactivity may contribute to the increase in sympathetic nerve activity (SNA) associated with diseases such as hypertension.
    AJP Regulatory Integrative and Comparative Physiology 05/2013; · 3.28 Impact Factor
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    ABSTRACT: It is widely accepted that the pathophysiology of hypertension involves autonomic nervous system dysfunction, as well as a multitude of immune responses. However, the close interplay of these systems in the development and establishment of high blood pressure and its associated pathophysiology remains elusive and is the subject of extensive investigation. It has been proposed that an imbalance of the neuro-immune systems is a result of an enhancement of the "proinflammatory sympathetic" arm in conjunction with dampening of the "anti-inflammatory parasympathetic" arm of the autonomic nervous system. In addition to the neuronal modulation of the immune system, it is proposed that key inflammatory responses are relayed back to the central nervous system and alter the neuronal communication to the periphery. The overall objective of this review is to critically discuss recent advances in the understanding of autonomic immune modulation, and propose a unifying hypothesis underlying the mechanisms leading to the development and maintenance of hypertension, with particular emphasis on the bone marrow, as it is a crucial meeting point for neural, immune, and vascular networks.
    Current Hypertension Reports 05/2013; · 3.90 Impact Factor
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    ABSTRACT: Background MicroRNAs (miRs), as essential gene expression regulators, modulate cardiovascular development and disease and thus they are emerging as potential biomarkers and therapeutic targets in cardiovascular disease, including hypertension. Methods and Results We assessed the expression levels of the microRNAs miR-9 and miR-126 in 60 patients with untreated essential hypertension and 29 healthy individuals. All patients underwent two-dimensional echocardiography and 24-h ambulatory blood pressure monitoring. MicroRNA expression levels in peripheral blood mononuclear cells were quantified by real-time reverse transcription polymerase chain reaction. Hypertensive patients showed significantly lower miR-9 (9.69±1.56 versus 41.08±6.06, p<0.001) and miR-126 (3.88±0.47 versus 8.96±1.69, p<0.001) expression levels compared with healthy controls. In hypertensive patients, miR-9 expression levels showed a significant positive correlation (r=0.437, p<0.001) with left ventricular mass index. Furthermore, both miR-9 (r=0.312, p=0.015) and miR-126 (r=0.441, p<0.001) expression levels in hypertensive patients showed significant positive correlations with the 24-h mean pulse pressure. Conclusions Our data reveal that miR-9 and miR-126 are closely related to essential hypertension in humans, as they show a distinct expression profile in hypertensive patients relative to healthy individuals and they are associated with clinical prognostic indices of hypertensive target organ damage in hypertensive patients. Thus, they may possibly represent potential biomarkers and candidate therapeutic targets in essential hypertension.
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