Neurohumoral regulation of blood pressure in rheumatic patients

Aim. To study characteristics of neurohumoral regulation of blood pressure (BP) in patients with systemic diseases of the connective tissue and hemorrhagic vasculitis (HV). Material and methods. The trial included 45 patients with systemic lupus erythematosus (SLE), 25 patients with scleroderma syst...

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Bibliographic Details
Main Authors: N P Shilkina, S A Stolyarova, I E Yunonin, I V Dryazhenkova, S E Stolyarova
Format: Article
Language:Russian
Published: "Consilium Medicum" Publishing house 2009-06-01
Series:Терапевтический архив
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Online Access:https://ter-arkhiv.ru/0040-3660/article/view/30363
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Summary:Aim. To study characteristics of neurohumoral regulation of blood pressure (BP) in patients with systemic diseases of the connective tissue and hemorrhagic vasculitis (HV). Material and methods. The trial included 45 patients with systemic lupus erythematosus (SLE), 25 patients with scleroderma systematica (SS), 30 HV patients and 30 healthy controls. The following parameters were estimated: activity of plasmic renin, aldosteron concentration in plasma, catecholamines (noradrenaline and adrenalin), serum level of endotheline-1, number of desquamated endotheliocytes by J. Hladovec (1978) with use of Goryaev's camera. A BP 24-h profile was obtained by the standard method with the device Kardiotekhnika 4000 AD. Renal function was assessed by blood creatinine (Reberg's test). Results. Contribution of different factors to pathogenesis of arterial hypertension (AH) in rheumatic conditions was different. SLE activity enhancement was associated with renal dysfunction and growth of plasmic renin leading to AH resultant from activation of the renin-angiotensin-aldosteron system (RAAS), sympathico-adrenal system (SAS) and suspended by endothelial dysfunction. AH in SS patients presented with SAS activation, endothelial dysfunction and moderate pathology of the kidneys. HV activation provoked renal and endothelial dysfunction, SAS activation leading to development of AH. Conclusion. In rheumatic diseases AH develops with activation of SAS, RAAS, endothelial and renal dysfunction.
ISSN:0040-3660
2309-5342