Vol 11, No 2 (2007)
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Published online: 2007-05-18

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The influence of blood pressure normalization on urotensin II and ghrelin levels in patients with primary hypertension. One-year follow-up

Małgorzata Kobusiak-Prokopowicz, Beata Jołda-Mydłowska, Monika Przewłocka-Kosmala, Maria Witkowska
Nadciśnienie tętnicze 2007;11(2):130-137.


Background Ghrelin (GR) is a peptide hormone that inhibits induces vasodilation, sympathetic nerve activity, apoptosis of cardiomyocytes and endothelial cells and improves cardiac function. Urotensin II (UII) is a vasoactive peptide with potent but highly variable vascular response. These properties indicate the fact that both peptides might be involved in pathophysiology of primary hypertension (HT). The aim of the study has been a UII and GR plasma level assessment in untreated hypertensive patients followed by evaluation of an impact of blood pressure normalization at these two neurohormones level during 12 month long treatment.
Material and methods A total of 70 untreated or ineffectively treated hypertensive patients were classified into groups of mild (HT-1), moderate (HT-2) and severe (HT-3) hypertension. 10 healthy persons served as a control group. An echocardiographic evaluation of left ventricular (LV) structure, systolic function and plasma level of both GR and UII by means of radioimmunoassay was performed in all patients and the control group. After 6 and 12 months of effective hypotensive treatment at patients with NT was repeated.
Results At baseline UII was significantly lower in HT-3 group than in controls and HT-2 (p < 0.05 and p < 0.007 respectively). GR in HT-2 and HT-3 groups was significantly lower while compared to both control group (p < 0.001) and HT-1 group (p < 0.04). After 12 months of treatment a decrease in UII plasma level in HT-2 group (p < 0.05) and decrease in GR plasma level in HT-1 and HT-2 groups (p < 0.05 and p < 0.01 respectively) were found. After 12-month treatment a significant negative correlation between GR level and LV mass index (r = –0.8, p < 0.001) was demonstrated. UII plasma level correlated with LV ejection fraction (r = 0.7, p < 0.02) and interventricular septum thickness (r = 0.8, p < 0.04), and in HT–3 group - with systolic blood pressure (r = 0.5, p < 0.002).
Conclusions 1. Negative corelation between GR and LV mass index and significantly lower GR in patients with more advanced HT indicate that GR depletion may contribute to HT pathophysiology. 2. Unequivocal changes of UII plasma level during hypotensive treatment together with its positive correlation with systolic blood pressure may be indicative of the peptide's contribution to pathophysiology of primary hypertension predominantly on tissue level.

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