Endothelium-dependent modulation of the pressor activity of XXXX in the isolated superior mesenteric arterial bed of the @entity35 .

@entity1831 @entity5463 @entity6693 @entity2604 @entity35 @entity3352 @entity1063
1. Pressor responses to @entity5463 ( @entity1831 ) were determined in the @entity35 isolated superior mesenteric arterial bed perfused with Krebs-Henseleit solution and compared with those to @entity1063 . 2. In control preparations the maximum pressor response to the peptide was 34 +/- 3 mmHg and the ED50 was 21 +/- 4 mu (n = 11). The maximal pressor response to @entity1063 (30 micrograms) 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 micrograms @entity1063 was unaffected. 3. @entity2604 (2.5 microM) significantly increased the maximum pressor response to AVP from 41 +/- 2 mmHg to 86 +/- 8 mmHg (n = 9); the ED50 was unchanged. @entity6693 (50 microM) 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 micrograms @entity1063 . 4. Neither @entity3352 (10 microM) nor BW755C (10 microM) had significant effects upon either the maximal response or ED50 for AVP nor did they affect the response to 10 micrograms @entity1063 . 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.
