Endothelium-dependent modulation of the pressor activity of arginine vasopressin in the isolated superior mesenteric arterial bed of the rat

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Abstract
1 Pressor responses to arginine vasopressin (AVP) were determined in the rat isolated superior mesenteric arterial bed perfused with Krebs-Henseleit solution and compared with those to noradrenaline. 2 In control preparations the maximum pressor response to the peptide was 34 ± 3 mmHg and the ED50 was 21 ±4mu (n = 11). The maximal pressor response to noradrenaline (30 μg) was 100 ± 6 mmHg (n = 8). After removal of the functional endothelium with the detergent CHAPS, the maximum pressor response to AVP increased to 64 ± 4 mmHg and the ED50 decreased to 7.7 ± 2.0 mu (n = 11) but the response to 10 μg noradrenaline was unaffected. 3 Nordihydroguaiaretic acid (2.5 μm) significantly increased the maximum pressor response to AVP from 41 ±2 mmHg to 86 ±8 mmHg (n = 9); the ED50 was unchanged. Methylene blue (50 μm) also increased the maximum response from 41 ± 3 mmHg to 87 + 13 mmHg (n = 8) without affecting the ED50. Neither treatment significantly affected the response to 10 μg noradrenaline. 4 Neither indomethacin (10 μm) nor BW755C (10 μm) had significant effects upon either the maximal response or ED50 for AVP nor did they affect the response to 10 μg noradrenaline. 5 In 6 preparations SKF-525A significantly increased both the ED50, from 9.8 ± 2.1 to 22 ± 2 mu, and the maximum response, from 36 ± 2 to 70 ± 3 mmHg. 6 It is concluded that the pressor response to AVP in this vascular bed is modulated, in the presence of functional endothelium, by the simultaneous release of endothelium-derived relaxing factor.