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The effect of HIV‐1 Tat on the aortic response to vasoconstrictors
Author(s) -
McDonough Kathleen H.,
Giaimo Mary,
Prakash Om
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.774.8
Subject(s) - phenylephrine , contraction (grammar) , immune system , chemistry , nitric oxide , genetically modified mouse , depolarization , inflammatory response , medicine , nitric oxide synthase , endocrinology , inflammation , pharmacology , immunology , transgene , biochemistry , blood pressure , gene
The human immunodeficiency virus (HIV‐1) has long term effects on the immune and cardiovascular systems. The HIV‐1 protein tat alters synthesis of proteins such as nitric oxide synthase and cytokines. The combination of alcohol (Alc) and Tat may exacerbate the effects of either Alc or Tat alone. We tested the hypothesis that Tat, expressed in transgenic mice, would depress aortic responses to constrictor agents and Alc would exacerbate this effect. To test this hypothesis, transgenic and control mice were given water or water with Alc (20% v/v) for 6‐8 weeks and then aortic ring contraction to depolarization with KCl and alpha mediated contraction with phenylephrine (PE) was determined. Some mice were given endotoxin (Endo) to simulate inflammation. Isolated rings from control mice increased tension in response to KCl and PE by approximately 75% and 92%, respectively. Similar changes were noted in the Tat control group. Alc increased the response of rings from control mice to KCl but not to PE. Alc increased the response to constrictors in the Tat mice in the opposite way ‐ increased response to PE but no change in response to KCl. 24 hr after Endo, the per cent change in tension was increased by PE but not by KCl. Results suggest that the major influence on constrictor tone was recovery from Endo rather than Tat or Alc provision. The Endo effect was primarily demonstrated by the increased response to PE, a receptor mediated process. (Supported by NIH AA013555)