Vol 9, No 2 (2005)
Original paper
Published online: 2005-04-11

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Analysis of vasoconstrictor responses to angiotensin II in rat isolated tail artery in experimental, chronic renal failure

Andrzej Brymora, Mariusz Flisiński, Grzegorz Grześk, Leszek Szadujkis-Szadurski, Jacek Manitius
Nadciśnienie tętnicze 2005;9(2):88-94.

Abstract

Background Recent studies indicate that arterial response to angiotensin II (ANG II) in chronic renal failure is variable. In our study we compared the response of rat tail artery to ANG II in different stages of chronic renal failure (CRF).
Material and methods Male 290–380 g Wistar rats were divided into three groups: 5/6 nephrectomy (n = 11), 3/4 nephrectomy (n = 9) and sham-operation (control n = 12). After 4 weeks blood pressure (BP) in carotid artery was measured and then the tail artery was excised. The proximal segment of artery was cannulated and mounted under 0.5 g tension in organic bath. The constriction of artery in response to ANG II was measured as an increased in perfusion pressure at a constant flow of the perfusion fluid. ANG II was applied into the extraluminal Krebs solution according to van Rossum method.
Results Both 3/4 and 5/6 nephrectomies leaded to development of CRF and hypertension — the CRF groups had significantly increased blood pressure, serum creatinine and BUN. The tail artery from rats after 3/4 nephrectomy was characterized by dicreased reactivity to Ang II (percent of maximal reaction) for concentration [M/L] 1 x 10–5 (12.7 ± 9.6 vs. 24.7 ± 7.4; p < 0.01) and 3 x 10–5 (16.9 ± 9.2 vs. 27.8 ± 12.7; p < 0.05). But the rat tail artery after subtotal nefrectomy (5/6) was characterized by hyperreactivity to ANG II comparing to control group. We found significant correlations for concentrations of ANG II: 1 x 10–5 (36.3 ± 12.6 vs. 24.7 ± 7.4; p < 0.05), 3 x 10–5 (39.4 ± 11.7 vs. 27.8 ± 12.7; p < 0.05), 1 x 10–4 (39.8 ± 11.9 vs. 28.7 ± 13.0; p < 0.05), 3 x 10–4 (40.1 ± 11.5 vs. 29,2 ± 12.9; p < 0.05).
Conclusion The arterial response to ANG II depends on a stage of chronic renal failure. Various arterial reactivity could be a result of changes in the affinity of the receptor to an agonist, or receptors concentration.

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