Enhanced skeletal muscle arteriolar reactivity to Ang II following recovery from ischemic acute renal failure
Basile, D.P.; Donohoe, D.; Frisbee, J.C.
FASEB Journal 17(4-5): Abstract
2003
ISSN/ISBN: 0892-6638 Accession: 034856586
We have demonstrated an enhanced pressor response following chronic infusion of Ang II in rats after recovery from acute renal failure (ARF). The present study assessed whether this augmented sensitivity was partially a function of altered reactivity of peripheral circulation to Ang II. Bilateral renal artery occlusion (45 min) followed by reperfusion in rats was utilized as a model of ARF. Evidence of injury and subsequent repair was verified by transient elevation of serum creatinine and histologic appearance of normal proximal tubular morphology at 5 weeks post injury. In study I, arterial pressure in conscious animals was not different between ARF and sham-operated controls at 5 weeks of recovery, however ARF-rats manifested an increased pressor sensitivity to acute graded doses of Ang II. At the highest doses of Ang II (50 ng/kg/min), the change in MAP was apprx2-fold greater vs. sham-operated controls. In study II, anesthetized rats at 5 wks recovery were used to study the reactivity of 3rd order arterioles of the in situ cremaster muscle. Ang II-induced vasoconstriction was enhanced in post-ischemic animals vs. shams, while responses to norepinephrine, O2, acetycholine and sodium nitropusside were not altered between the two rat groups. These data suggest that a predisposition to elevated arterial pressure following recovery from ARF is associated with enhanced peripheral vascular sensitivity to Ang II.