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Effects of angiotensin II on resistance vessels in hamster hypertension
Author(s) -
Kurjiaka David T.,
Burt Janis M.
Publication year - 2008
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.22.1_supplement.968.11
Subject(s) - medicine , endocrinology , constriction , angiotensin ii , losartan , endothelin 1 , blood pressure , chemistry , renin–angiotensin system , endothelin receptor , biology , receptor
Earlier work suggested endothelin‐1 elevated blood pressure in the spontaneously hypertensive hamster (SHH). However, while no differences were observed in vascular responses to endothelin‐1, maximal angiotensin II (Ang II) constriction was greater in the SHH (75% vs 50% normotensive). Interestingly, the potent constrictor was <100% effective in both strains. These experiments investigated this incomplete Ang II constriction in the SHH. In isolated skeletal muscle feed arteries, Ang II constriction was unaltered by the AT‐2 antagonist PD‐123319 (4 μM). Rather, maximal constriction to Ang II were recovered by angiotensin converting enzyme 2 (ACE2) inhibition with DX‐600 (0.1 μM) such that no differences were observed between strains. This suggests that earlier differences in Ang II constriction reflected a reduced ACE2 activity in resistance vessels of the SHH. Since the Ang 1–7 generated by ACE2's action on Ang II did not relax these vessels, the reduced constriction would appear to involve a decrease in Ang II rather than an increased Ang 1–7 action. Interestingly, ACE2 expression was greater in the SHH suggesting that ACE2 activity is dramatically reduced in the SHH. As the elevated blood pressure was completely recovered by acute application of losartan (60 mg/kg), the elevated blood pressure in the SHH appears to result from reductions in ACE2 activity that would increase local concentrations of Ang II.