Angiotensin II type 1 (AT1) receptor blockade enhances the L-NAME-induced vasoconstriction in rat submandibular gland

• Published in: Experimental physiology 2002-05, Vol.87 (3), p.327-333
• Main Authors: Vág, J., Kerémi, Beáta, Hably, Csilla, Bartha, J., Fazekas, Á.
• Format: Article
• Language: English
• Subjects: Angiotensin Receptor Antagonists; Animals; Benzimidazoles - pharmacology; Blood Pressure - drug effects; Enzyme Inhibitors - pharmacology; Full Length Papers; Heart Rate - drug effects; Laser-Doppler Flowmetry; Male; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase Type III; Rats; Rats, Wistar; Receptor, Angiotensin, Type 1; Regional Blood Flow - drug effects; Rubidium Radioisotopes; Submandibular Gland - blood supply; Submandibular Gland - drug effects; Tetrazoles - pharmacology; Vasoconstriction - drug effects
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/eph8702330

The vasoregulatory role of nitric oxide (NO) and angiotensin II type 1 (AT1) 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 AT1 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 AT1 receptors. These findings suggest that the AT1 receptors have an important role in the vasoregulation of the SMG in the rat. As a result of AT1 blockade, NO-dependent tone of glandular vessels may be enhanced significantly. Experimental Physiology (2002) 87.3, 327-333.