Hypertension, transmural pressure, and vascular smooth muscle response in rats.

Abstract

The effect of transmural pressure on the responsiveness of vascular smooth muscle was studied using rats with chronic occlusion of one external iliac artery. The arterial pressure in the occluded leg was reduced to approximately half of that in the contralateral unoccluded leg. Helical strips from the low-and high-pressure femoral arteries of spontaneously hypertensive rats and rats with deoxycorticosterone acetate-induced (DOCA) hypertension were compared with corresponding tissues from normotensive controls. The sensitivity of both low-and high-pressure artery strips from the spontaneously hypertensive rat was greater than that of control? when strontium or lanthanum was used as the agonist. The sensitivity of strips from both low-and high-pressure arteries from the DOCA-hypertensive rat was greater than that of controls when potassium, epinephrine, or calcium was the agonist. There was no difference in sensitivity between strips from the low-and high-pressure arteries in any group of rats. Maximum contractile force (contractility) was reduced in femoral artery strips from both legs of all hypertensive rats. The KCl-induced contraction of vascular smooth muscle from both femoral arteries of either form of hypertensive rat was not as readily depressed by high calcium concentrations as was that from the normotensive rat. Changes in sensitivity and contractility associated with hypertension could not be reversed by lowering blood pressure in one leg of a spontaneously hypertensive rat or prevented by protecting one leg from high pressure prior to the induction of DOCA hypertension. The altered sensitivity and contractility of arterial strips in these models of hypertension are not, then, secondary to the increase in wall stress. KEY WORDSsmooth muscle contractility smooth muscle sensitivity spontaneously hypertensive rats potassium DOCA-hypertensive rats lanthanum strontium calcium depression of KC1 contraction epinephrine• Extensive evidence from studies of perfused vessels (1) or vascular beds (2-7) as well as from studies of isolated vascular smooth muscle (8)(9)(10)(11)(12)(13) indicates that vascular responsiveness is increased in hypertension. A reasonable inference from this evidence is that the increase in responsiveness causes the elevated total peripheral resistance that results in hypertension. However, in view of recent findings showing that the increased wall stress of hypertension can produce profound adaptive changes in the artery wall (5, 14-16), more definitive evidence is needed to determine whether the increased responsiveness of vascular smooth muscle in the hypertensive rat occurs in the absence of increased wall stress. This study was supported in part by U. S. Public Health Service Grant HL-03756 from the National Heart and Lung Institute. Dr. Hansen was supported by NIH Training Grant GM-00353.Dr. Hansen's present address is Department of Physiology, Harvard Medical School, Boston, Massachusetts 02155.Received March 14, 1974. Accepted for publication February 12, 1975. This stu...

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