Regression of Structural Cardiovascular Changes after Reversal of Experimental Renal Hypertension in Rats

Renal hypertension was induced in young normotensive male Wistar rats by constriction of one renal artery. This constriction was released 3–4 weeks later when pressure had stabilized around 180 mm Hg and when the structural cardiovascular adaptation to this hypertensive level was largely completed (Folkow et al . 1973, Lundgren et al . 1974). 1, 3, 7, 14 and 25 days later paired hindquarter perfusions were performed on one declipped renal hypertensive rat (D‐RHR) and one normotensive control rat (NCR), exploring the design of the resistance vessels as expressed by the resistance at maximal vasodilatation, the maximal slope of the dose‐response curve to noradrenaline and the maximal pressor response (cf . Folkow et al . 1970 b). At the same time intervals the left heart ventricles of all animals were weighed. Already one day after declipping, arterial pressure was normalized while the hemodynamic analysis indicated that the D‐RHR resistance vessels, like the left ventricle, still showed largely unchanged hypertrophic changes characterizing hypertension. Then, however, a rapid regression of these changes occurred, being considerable already after 7–14 days, and after about 3 weeks the design of both heart and resistance vessels had become fully readapted to normotensive levels.