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Am J Physiol Regul Integr Comp Physiol (August 19, 2004). doi:10.1152/ajpregu.00178.2003
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Submitted on April 4, 2003
Accepted on August 11, 2004

DO INCREMENTAL INCREASES IN BLOOD PRESSURE ELICIT NEOINTIMAL PLAQUES THROUGH ENDOTHELIAL INJURY?

Ciro A Ruiz-Feria1, Yimu Yang1, and Hiroko Nishimura1*

1 Physiology, University of Tennessee Health Science Center, Memphis, TN, USA

* To whom correspondence should be addressed. E-mail: nishimur{at}physio1.utmem.edu.

Fowl (males more so than females) show maturation-dependent rises in blood pressure (BP) and formation of neointimal plaques (NPs), resembling balloon-catheter injury-induced neointima, in the abdominal aorta (AbA) just above the bifurcation. The plaque comprises neointimal cells containing abundant endoplasmic reticulum and abundant extracellular matrix. Hence, we investigated whether rapid incremental increases in BP in male chicks trigger NP formation, possibly via endothelial injury in hemodynamically selective areas. In 6-wk-old chicks (n = 8) treated 4 wks with solvent (Sv, minipump) or arginine supplement (Arg, 0.3% in drinking water), BP increased from 140 ± 5 to 159 ± 4 mm Hg (Sv) and from 138 ± 4 to 157 ± 3 (Arg), whereas propranolol treatment (Prop, 8 mg/kg/d; minipump) prevented the rise. Arg and Prop groups had, respectively, 73 and 77% smaller (P < 0.05) NP areas and 19 and 25% less (P < 0.01) AbA medial thickness than Sv controls. In 16-wk-old cockerels, the established BP remained high after Sv and Arg treatments. In the Prop group, BP decreased; but neither the NP area nor the medial thickness was lower than in the Sv group, whereas the Arg group showed greater NP area and medial thickness. Pulse pressure, determined by intravascular transducer, increased as the pulse wave descended the aorta. The results suggest that maturation-dependent rises in BP in chicks may trigger NP formation in the lower segment of the AbA, which was prevented by inhibition of BP-increase, or via a possible increase in nitric oxide availability. BP reduction exerts no effect once BP reaches a plateau. Involvement of endothelial injury leading to NP formation and the hemodynamic forces selective to the lesion-prone area remain to be determined.







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