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The immunological basis of hypertension
#MMPMID25150828
Rodríguez-Iturbe B
; Pons H
; Quiroz Y
; Johnson RJ
Am J Hypertens
2014[Nov]; 27
(11
): 1327-37
PMID25150828
show ga
A large number of investigations have demonstrated the participation of the
immune system in the pathogenesis of hypertension. Studies focusing on
macrophages and Toll-like receptors have documented involvement of the innate
immunity. The requirements of antigen presentation and co-stimulation, the
critical importance of T cell-driven inflammation, and the demonstration, in
specific conditions, of agonistic antibodies directed to angiotensin II type 1
receptors and adrenergic receptors support the role of acquired immunity.
Experimental findings support the concept that the balance between T cell-induced
inflammation and T cell suppressor responses is critical for the regulation of
blood pressure levels. Expression of neoantigens in response to inflammation, as
well as surfacing of intracellular immunogenic proteins, such as heat shock
proteins, could be responsible for autoimmune reactivity in the kidney, arteries,
and central nervous system. Persisting, low-grade inflammation in these target
organs may lead to impaired pressure natriuresis, an increase in sympathetic
activity, and vascular endothelial dysfunction that may be the cause of chronic
elevation of blood pressure in essential hypertension.
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