SUMMARY 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 n (Ang II) reactivity before and 10 to 14 days after Grolhnan (two-kidney, one figure-8) or sham operation. Mkrovascular 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* pmol) and venules (10"' pmol) in 10-/tl abquots 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 H) 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. and that the latter only occurs in later stages of hypertension.2 Furthermore, there is a greater dissipation of microvascular pressure in the hypertensive compared to the normotensive hamster despite the absence of changes in wall thickness. Although in the rat the chronic phase of onekidney, one figure-8 hypertension is characterized