Vasodilators, Aortic Elasticity, and Ventricular End-Systolic Stress in Nonanesthetized, Unrestrained Rats

We evaluated the effect of different vasodilators on ventricular end-systolic stress by investigating the impact of sodium nitroprusside, nifedipine, and hydralazine on blood pressure, aortic stiffness, and wave reflection during drug-induced hypotension (to 80 mm Hg mean blood pressure) in normotensive (central aortic mean blood pressure, 116 to 119 mm Hg; systolic pressure, 133 to 137 mm Hg), nonanesthetized, unrestrained rats. Aortic stiffness was evaluated from the slope of the linear regression relating pulse wave velocity (PWV) to central aortic mean or pulse pressure. The fall in central aortic systolic blood pressure was less than the fall in mean pressure, especially after hydralazine (122 +/- 4 mm Hg; sodium nitroprusside, 107 +/- 2; and nifedipine, 112 +/- 3 mm Hg; P < .05). The PWV/mean pressure slope was linear, positive, and similar in all three groups (hydralazine, 3.3 +/- 0.2; sodium nitroprusside, 3.8 +/- 0.3; and nifedipine, 3.9 +/- 0.3 cm [center dot] s [center dot] mm Hg; P > .05). The PWV/pulse pressure slope was linear, negative, and less steep in the case of hydralazine (-4.9 +/- 0.6; sodium nitroprusside, -15.5 +/- 3.7; and nifedipine, -13.5 +/- 2.9 cm [center dot] s [center dot] mm Hg; P < .05). The travel time and augmentation index of the reflected wave were similar in all groups. In conclusion, sodium nitroprusside and nifedipine had a more beneficial effect on end-systolic stress than did hydralazine. This does not appear to be related to any specific effect on wave reflection or the "static" relationship between PWV and aortic mean blood pressure; it may be related to the effects of these drugs on the "dynamic" relationship between PWV and pulse pressure. (Hypertension. 1997;30:1169-1174.)