Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Abstract

Vessel dimensions and characteristic responses to norepinephrine were measured in various arteries and veins of the rabbit made hypertensive by partial constriction of the upper abdominal aorta. The ear, radial, and basilar arteries taken from the circulation proximal to the ligature (the hypertensive arteries) were thickened in proportion to the rise in arterial blood pressure. The water, sodium, and potassium contents of these and all other vessels were not significantly changed in the hypertensive rabbits. The maximum response to norepinephrine in the ear artery, a representative vessel from the hypertensive part of the rabbit, was increased, whereas the sensitivity of this vessel to norepinephrine expressed as the ED 50 did not alter with changes in the arterial blood pressure. In contrast, the thickness and the maximum response to norepinephrine of the saphenous artery, representative of vessels distal to the ligature (normotensive vessels) and of the saphenous and cephalic veins were unaltered. The sensitivity as indicated by the norepinephrine ED 50 of the veins, but not of the saphenous artery, increased with a rise in carotid artery blood pressure. These results suggest that the increased responsiveness to norepinephrine of arteries proximal to the ligature is due to changes in muscle mass and that the increased responsiveness of the veins is due to increased sensitivity to norepinephrine.• The analysis of changes in responsiveness of blood vessels in hypertensive animal models has been the object of many investigations (1-14). A critical survey of these studies led us to define five experimental objectives, which served as the incentive for the present series of experiments. We wanted (1) to accurately determine the effect of hypertension on the responsiveness of vessels to norepinephrine in vitro using vessel rings; (2) to study a variety of vessels, including elastic and muscular arteries and veins, and (3) to separate local consequences of an increased intravascular pressure on the blood vessel wall from any generalized effects associated with the hypertensive state. We felt that (4) small early changes in the vessel wall should be observed if possible, since they are particularly relevant to the genesis of hypertension and that (5) control animal selection should minimize individual variation so that the small changes consequent to the hypertensive state could be recognized.The experimental model of hypertension which we chose to study was the rabbit with its abdominal aorta partially constricted between the celiac and anterior mesenteric arteries (15)(16)(17). In this preparation, after a few days the pressure in the arterial circulation proximal to the ligature becomes raised and that distal to the ligature returns to within the normal range. Although not all of our objectives were realized, many were satisfied by this approach. Existing techniques allowed measurements of vessel responsiveness to norepinephrine in both arteries and veins (18,19). A comparison of the changes in vessels tak...

Relationship Between Neointimal Thickness and Shear Stress After Wallstent Implantation in Human Coronary Arteries

“…In our range of curvatures and vessel diameters, we estimate this difference as Ͻ10%, which is far less than the observed difference in SS between inner and outer curves (by a factor of 2). In addition, because the observed relation between vessel wall thickness and wall stress 24 is linear, we do not expect that a 10% wall stress variation will produce a 100% variation in neointimal hyperplasia.…”

Vascular responses of the perfused intestine to vasoactive agents during the development of two-kidney, one-clip Goldblatt hypertension in dogs.

“…48, No. 6, JUNE 1981 indicate that early vascular reactivity changes may occur independent of pressure changes since (1) enhanced vascular reactivity precedes the increased arterial resistance of various models of experimental hypertension and (2) the study of veins in hypertension demonstrates that venous smooth muscle is less compliant, hypertrophied, and may demonstrate enhanced contractility (Bevan et al, 1976;Greenberg and Bohr, 1975;Takeshita and Mark, 1978;Greenberg et al, 1978). Folkow et al (1970) have presented evidence indicating that most, if not all, of the increased vascular resistance and reactivity in the established phase of experimental and human essential hypertension is caused by an increased vascular wall thickness.…”

Cardiovascular hypertrophy and "waterlogging" in coarctation hypertension. Role of sympathoadrenergic influences and pressure.

“…Cellular hypertrophy or hyperplasia would explain the increases in potassium content in the aorta in coarctation hypertension observed by Pamnani and Overbeck. On the other hand, Bevan et al, 16 studying coarctation hypertension in rabbits, found no evidence for growth of the abdominal aorta. This group also found no changes in water and electrolyte content Of arterial wall, not even in the hypertensive portions of the vascular bed, 16 suggesting that basic disease mechanisms of coarctation hypertension may be different in rabbits and rats.…”