Urotensin II and ghrelin and target organ damage in primary hypertension

Background Ghrelin (GR) is a peptide hormone that induces vasodilation, inhibits sympathetic nerve activity, apoptosis of cardiomyocytes and endothelial cells, and improves cardiac function. Urotensin II (UII) is another vasoactive peptide with potent but highly variable vascular response. These findings raised the possibility that both peptides play a role in maintaining vascular tone and therefore may be involved in pathophysiology of primary hypertension. We investigated the relationship between plasma levels of GR and UII and arterial blood pressure (BP) as well as left ventricular (LV) structure in patients with different stages of hypertension (HT). Material and methods A total of 70 hypertensive patients (HTpts) were classified in groups of mild (1), moderate (2) and severe (3) HT and divided into group without organ damage (A), with sign of organ damage (B) and group C with stable coronary artery disease (CAD). In all patients and controls echocardiographic examination of LV structure and systolic function was performed. Plasma level of GR and UII were measured using RIA Peninsula Lab. Inc. Results GR level in groups 2 and 3 HT was significantly lower compared to controls (p < 0.001) and groups 1 HT (p < 0.04) and in HTpts of group B and C compared to controls or group A (p < 0.05). Significant negative correlation between GR level and SBP (r = -0,36, p < 0,05), DBP (r = -0,39, p < 0,002), LV mass (r = -0,37, p < 0,006) and LV mass index (r = -0,46, p < 0,03) were found out. Plasma UII level in group 3 HT and A was significantly lower compared to controls and 2 HTpts (p < 0.007). UII level correlated only with z SBP (r = -0.256, p < 0.004). Conclusions Decreased level of GR in HTpts and significant inverse correlation between GR level and LV mass index suggest GR involvement in pathogenesis of HT and target organ damage as a result of imbalance in vasorelaxative and vasoconstrictive action with predominance of the last. Diminished UII level in pts with severe HT as compared with controls may indicate significance of tissue but not plasma expression of UII in this stage of HT.