Changes of Some Humoral Factors, Playing Role in the Pathogenesis of Hypertension in Acromegaly

Author: E. Natchev, G.Kirilov, I. Atanasova, J. Matrozova, K. Kalinov, S. Zacharieva

Abstract:

A high prevalence of hypertension (HTN) in acromegaly has been reported. Different mechanisms, which have not been clearly elucidated yet, participate in the pathogenesis of HTN in acromegalic patients.

 

Aim. To determine the prevalence of HTN in acromegalic patients; to investigate the relationship between the disease activity in acromegaly and HTN; to investigate the changes in some humoral factors, playing role in the pathogenesis of HTN and in the alteration of the vessel wall (active renin (AR), aldosterone, Prostaglandine E2 (PgE2), Vascular Endothelial Growth Factor (VEGF).

 

Patients and methods. The study population consisted of 61 patients with acromegaly, divided into 2 groups (41 with active acromegaly and 20 patients witn nonactive acromegaly) and each group was divided into 2 subgroups- with or without HTN. These cases were compared with 41 healthy controls and 117 controls with essential HTN. Growth hormone was measured by fluorometric assay and active renin- by IRMA. Aldosterone was measured by radioimmunoassay. PGE2 and VEGF were measured using ELISA method.

 

Results. А high prevalence of HTN was found in acromegalic patients – 54,1%. There was no statistically significant relationship between the activity of acromegaly and HTN. We found a lower active renin in patients with acromegaly without HTN compared to healthy controls, possibly explained by the state of hypervolemia. Also, a higher active renin was found in acromegalic hypertensive patients, compared to patients with essential HTN. Aldosterone was higher in patients with acromegaly and HTN, compared to patients with acromegaly without HTN. We found a higher aldosterone/active renin ratio in patients with active acromegaly. This is in favour of a relative activation of the reninangiotensin- aldosterone system (RAAS) in relation to the state of hypervolemia in patients with acromegaly. We found lower levels of PgE2 in patients with acromegaly compared to healthy controls as well as a tendency to lower levels in active acromegaly. There was no difference in levels of VEGF in patients with acromegaly (in the whole population or in patients without HTN) compared to healthy controls, or in acromegalic hypertensive patients compared to patients with acromegaly without HTN.

 

Conclusions. Acromegaly is associated with a higher prevalence of HTN. There is no significant relationship between the activity of acromegaly and HTN. RAAS is relatively activated in relation to hypervolemia and PGE2 is suppressed, and possibly both of them participate in the pathogenesis of HTN in acromegaly. Probably VEGF does not participate in pathologic changes in acromegaly (HTN, vessel alteration, tumorogenesis).