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Hypertension. 1988;12:373-379

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Hypertension, Vol 12, 373-379, Copyright © 1988 by American Heart Association


ARTICLES

Angiotensin reactivity in the cheek pouch of the renovascular hypertensive hamster

TO Myers, WL Joyner and JP Gilmore
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha 68105-1065.

Increased reactivity to vasoconstrictor agents and decreased arteriolar luminal diameter have been implicated in the maintenance of hypertension. The same hamster cheek pouch microvessels were tested for angiotensin I (Ang I) and angiotensin II (Ang II) reactivity before and 10 to 14 days after Grollman (two-kidney, one figure-8) or sham operation. Microvascular geometric parameters were measured before and after a maximal vasodilator dose of adenosine. Then maximal vasoconstrictions to Ang I or Ang II were measured: Ang I and Ang II were applied adjacent to arterioles (10(-2)-10(0) pmol) and venules (10(-1) pmol) in 10-microliter aliquots for 1 minute. Blood pressure (178 +/- 11/133 +/- 8 mm Hg) of renovascular hypertensive hamsters was elevated significantly over blood pressure of sham-operated hamsters (120 +/- 11/97 +/- 10 mm Hg). No change was observed in venular geometry or reactivity in renovascular hypertensive hamsters. Arteriolar luminal diameter, wall thickness, wall/lumen ratio, and wall area were not altered in hypertensive hamsters in the normal or vasodilated state; vasodilator capacity was the same in all groups. Conversion of Ang I to Ang II (response to Ang I divided by response to Ang II) for first-order and Third-order arterioles and third-order venules was 74 +/- 5, 79 +/- 3, and 72 +/- 6%, respectively, and was unaltered in renovascular hypertensive hamsters. Although vessel geometry was not altered, there was a significant shift to the left of the Ang I and Ang II dose-response curves of first-order and third- order arterioles, indicating increased sensitivity to these vasoconstrictors.(ABSTRACT TRUNCATED AT 250 WORDS)


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