Angiotensin II type 1 (AT(1)) receptor blockade enhances the L-NAME-induced vasoconstriction in rat submandibular gland.

The vasoregulatory role of nitric oxide (NO) and angiotensin II type 1 (AT(1)) receptors in the circulation of the submandibular gland (SMG) of rats was studied. The glandular blood flow was determined by means of laser Doppler flowmetry and rubidium isotope technique. The data obtained by these two methods correlated well (r = 0.77; P < 0.01). The AT(1) receptor antagonist candesartan (0.5 mg kg(-1), i.v.) reduced the vascular resistance in the SMG by 37 % (P < 0.05). By contrast, the NO synthase blocker L-NAME (15 mg kg(-1), i.v.) significantly increased vascular resistance in the SMG both in candesartan-treated (P < 0.001) and non-treated (P < 0.001) animals. The increase in resistance was greater (P < 0.05) after previous blockade of AT(1) receptors. These findings suggest that the AT(1) receptors have an important role in the vasoregulation of the SMG in the rat. As a result of AT(1) blockade, NO-dependent tone of glandular vessels may be enhanced significantly.