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Endothelium‐dependent modulation of the pressor activity of arginine vasopressin in the isolated superior mesenteric arterial bed of the rat
Author(s) -
Randall Michael D.,
Kay Alexander P.,
Hiley C. Robin
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11687.x
Subject(s) - pressor response , vasopressin , endocrinology , medicine , arginine , vasoconstriction , norepinephrine , chemistry , endothelium , blood pressure , heart rate , amino acid , dopamine , biochemistry
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 ED 50 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 ED 50 decreased to 7.7 ± 2.0 mu ( n = 11) but the response to 10 μg noradrenaline was unaffected. 3 Nordihydroguaiaretic acid (2.5 μ m ) significantly increased the maximum pressor response to AVP from 41 ±2 mmHg to 86 ±8 mmHg ( n = 9); the ED 50 was unchanged. Methylene blue (50 μ m ) also increased the maximum response from 41 ± 3 mmHg to 87 + 13 mmHg ( n = 8) without affecting the ED 50 . Neither treatment significantly affected the response to 10 μg noradrenaline. 4 Neither indomethacin (10 μ m ) nor BW755C (10 μ m ) had significant effects upon either the maximal response or ED 50 for AVP nor did they affect the response to 10 μg noradrenaline. 5 In 6 preparations SKF‐525A significantly increased both the ED 50 , 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.