In Vitro Demonstration of Vascular Hyper-responsiveness in Experimental Hypertension
The ventral caudal artery from DCA hypertensive and control rats was excised, mounted in a plastic chamber, and perfused with Krebs-Henseleit solution. Diameter of the artery and flow through the artery were measured at perfusion pressures ranging from 0 to 150 mm Hg. During these perfusions, constriction of the arterial segment was produced by adding norepinephrine, vasopressin, angiotensin II or rat serum in concentrations known to produce submaximal contractions.
Samples of each experimental artery before and after artificial perfusion were fixed, sectioned, and stained. The tunica media of hypertensive arteries was thickened. Also, degenerative changes were observed in the internal elastic lamina and adjacent tunica media. Structural thickening of the tunica media was due primarily to expansion of the extracellular space and also due possibly to muscle fibre hypertrophy.
In the absence of contraction, flow through the hypertensive artery was moderately reduced at all pressures because its lumen was narrowed by the thickened wall.
Total wall tension, muscle tension, and elastic tension of the artery were estimated from the pressure-flow-radius data. Strength of muscular contraction was then measured in terms of work performed during contraction at a constant pressure. From this analysis, the muscle fibres in hypertensive arteries were found to be unequivocally hyper-responsive to norepinephrine, vasopressin, and rat serum. The possible cause of this hyper-responsive property is discussed.
Serum was collected both from normotensive and from hypertensive donor rats and its pressor activity tested on the in vitro preparation. The pressor activity in hypertensive serum was found to be significantly elevated.
The elasticity of the hypertensive artery was increased in the absence of contraction and unchanged during contraction. No hypertensive artery was found to be stiffer than normotensive arteries. These changes are probably related to degeneration of elastin.
- Accepted April 26, 1965.
- © 1965 American Heart Association, Inc.