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Stimulation of vascular glycosaminoglycan synthesis by subpressor angiotensin II in rats.
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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 35SO4 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.min-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 glycosaminoglycans in the aorta was proportionately increased by Ang II. The early occurrence, magnitude, and arterial pressure independence of Ang II-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.
Title: Stimulation of vascular glycosaminoglycan synthesis by subpressor angiotensin II in rats.
Description:
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 35SO4 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.
min-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 glycosaminoglycans in the aorta was proportionately increased by Ang II.
The early occurrence, magnitude, and arterial pressure independence of Ang II-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.
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