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Stimulation of Vascular Glycosaminoglycan Synthesis by Subpressor Angiotensin II in Rats

The vascular trophic effects of angiotensin II (Ang II) in small doses may precede its hypertension-producing effect, and de novo synthesis of components of extracellular matrix may be a requirement for Ang II-stimulated growth. In the present study, therefore, the incorporation of 35SC4 into glycosaminoglycans (synthesis) of aorta and bladder wall of young adult, male Sprague-Dawley rats was measured ex vivo after 48 hours of Ang II administration at two dose levels, 100 and 200 ng · kg−1 · min−1 IP. Vehicle-infused rats served as controls. Compared with controls, systolic blood pressure was unchanged in rats receiving 100 ng · kg−1 · min−1 Ang II and rose by 13 mm Hg (P<.05) in rats receiving the 200- ng · kg−1 · rain−1 dose. In Ang II-treated rats, glycosaminoglycan synthesis of the aorta was increased by 20% (P<.05) and 52% (p<.005) at the two dose levels, respectively. Glycosaminoglycan synthesis of bladder smooth muscle was also increased in Ang II-treated rats (P<.01), but the response was not dose dependent. By 7 to 10 days of Ang II administration (200 ng · kg−1 · min−1), glycosaminoglycan synthesis of aorta returned toward baseline (P<.10, >.05). The rate of synthesis of subtypes of glycosaminogrycans in the aorta was proportionately increased by Ang II. The early occurrence, magnitude, and arterial pressure independence of Ang H-induced glycosaminoglycan synthesis suggest that restructuring of extracellular matrix may play an important role in both the trophic and hypertension-producing action of Ang II.