Although the angiotensin II (AngII)/AT1 receptor system is best known for mediating blood pressure and body water/electrolyte balance it also facilitates tumor vascularization and growth by stimulating the expression of VEGF.
These results could, at least in part, contribute to the discussion about the possible effects of ACE inhibitors and AT1 receptor antagonists in malignancy, and offer new clues to support their use for tumor control.
In contrast to captopril challenge, PRA was suppressed by 30% in Case 1 and 42% in Case 2 in response to saline infusion, and was increased by 230% in Case 1 and 59% in Case 2 in response to furosemide-upright posture for 2 h. These results suggest that the short loop feedback inhibition of renin secretion by Ang II in JG cell tumor is closely related to AT1 receptor expression levels in the tumor tissue.
In addition, polymorphic subtypes of AT1 receptor do not seem to play a major role in the pathogenesis of these tumors, even though a tendency towards a higher frequency of the polymorphic base substitution at position 573 (T573-->C) in cortisol-producing tumors needs to be further evaluated.
In patients with aldosterone-producing adenomas either responsive or unresponsive to the renin-angiotensin system, no differences were detected using SSCP analysis in the coding region of the AT1 receptor gene in peripheral blood or tumour tissue.