[Arg(8)]-vasopressin-induced responses on coronary and mesenteric arteriesof rats with myocardial infarction: The effects of V-1a- and V-2-receptor antagonists

Citation
Im. Lankhuizen et al., [Arg(8)]-vasopressin-induced responses on coronary and mesenteric arteriesof rats with myocardial infarction: The effects of V-1a- and V-2-receptor antagonists, J CARDIO PH, 36(1), 2000, pp. 38-44
Citations number
42
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
ISSN journal
01602446 → ACNP
Volume
36
Issue
1
Year of publication
2000
Pages
38 - 44
Database
ISI
SICI code
0160-2446(200007)36:1<38:[ROCAM>2.0.ZU;2-X
Abstract
After myocardial infarction, plasma levels of \ Arg(8)\-vasopressin rise to recover hemodynamics. The vascular responses to \ Arg(8)\-vasopressin were studied in vitro in isolated hearts and mesenteric artery segments of rats with 1-day and 3-week-old infarcts, in absence and presence of the V-1a-re ceptor antagonist SR-49059 and the V-2-receptor antagonist OPC-31260. Vascu lar responses of coronary arteries were similar in sham and infarcted heart s. On average, coronary flow was maximally decreased by 70 +/- 3% from base line values of 11.1 +/- 0.3 ml/min, with pD(2) values of 10.52 +/- 0.05. In mesenteric artery segments of sham and infarcted rats, maximal contractile forces, expressed as percentage of contraction to 125 mM KCl, were similar (232 +/- 23% and 239 +/- 8%, respectively). However, pD(2) values from inf arcted rats (9.22 +/- 0.07) were significantly lower compared with sham (9. 55 +/- 0.07) rats, In coronary as well as mesenteric vessels, the vasoconst rictor responses, being more susceptible to SR-49059 (apparent pA(2), betwe en 9.12 and 9.82) than to OPC-31260 (apparent pA(2), between 6.21 and 6.92) , seemed mediated by the V-1a receptor. These data indicate that in mesente ric but not in coronary vessels, an altered responsiveness to vasopressin c ould be observed. Responses are mediated mainly by the V-1a receptor.