Endocrine Abstracts

Introduction: Vasovagal syncope (VVS) is a transient loss of conscioussness due to hypoperfusion of the brain caused by vasodepressoric and/or cardioinhibitory reflex. In the pathogenesis, a dysregulation of autonomic nervous system is playing an important role. There is a growing evidence about more complex neurohumoral background of VVS. Neuropeptide Y (NPY) is hormone involved in the regulation of blood pressure with potent vasoconstriction effect. Moreover, NPY is also a cotransmitter with noradrenaline in sympathetic nervous system and is considered to be involved in sympathetic-induced vasoconstriction. Other vasoacitve hormones such as endothelin (ET-1) and angiotensin (ANG) can be implicated in pathogenesis of VVS, too.

Aim: The aim of this study was to evaluate the serum levels of NPY before and after head up tilt test (HUTT) and to compare them between patients with tilt induced VVS and group of negative individuals. Second aim was to find a correlation between NPY and other vasoactive hormones – ET-1 and ANG.

Subjects and methods: Altogether 69 subjects were included in this preliminary study (age 39+3,2 years; 41 females) with the history of at least one syncope. HUTT was performed in all subjects according to Italian protocol (20 minutes of passive standing followed by 15 minutes lasting phase after provocation by sublingual nitroglycerin). According to the result of HUTT, patients were divided into HUTT-positive (HUTT+) and HUTT-negative (HUTT-) group. Blood samples were collected before and immediately after HUTT. Serum levels of NPY, ET-1 and ANG were evaluated by ELISA method.

Results: HUTT was positive in 60 patients (HUT+ group), 29 subjects were negative (HUT-). There was no significant difference in basal levels of NPY between HUTT+ and HUTT- group (36.4+2.4 vs 40.1+1.5 ng/ml, P=0.1, T = 1.5). The stimulated levels of NPY were significantly lower in HUT+ patients when compared to HUT- (36.7+2.1 vs 44.4+3.2 ng/ml, P=0.028, T = 2.0). Both subgroups did not differ in ET-1 and ANG levels. Stimulated NPY levels positively correlated with stimulated ET-1 (P=0.001; R2=0.16) and ANG (P=0.04; R2=0.06) in all subjects. When divided into HUT+ and HUT-, NPY significantly correlated only with ANG (P=0.004; R2=0.4) in HUT- group, while in HUT+ patients, there was a positive correlation with ET-1 (P=0.0009; R2=0.23) found.

Conclusion: The impaired release of NPY may play a role in pathogenesis of VVS. Other vasoconstrictive hormones, such as ET-1 and ANG, can be involved in pathomechanisms, too.