Effect of sodium, deoxycorticosterone and duration of hypertension on pressor responses in rats

1. Enhanced pressor responsiveness to angiotensin II and noradrenaline has been demonstrated in the hypertension that follows deoxycorticosterone (DOC) and salt administration in the rat. The present studies were carried out to assess the importance of factors common to both pressor agents and those specific to individual agents such as receptor availability.2. Accordingly pressor reponses to angiotensin II and noradrenaline have been studied in normotensive salt-loaded and sodium depleted rats with and without DOC, and in rats with DOC-salt hypertension of short and long duration. These responses have been related to the plasma renin levels in the animals studied.3. Pressor reponses to angiotensin II were increased, dose-response curve (d.r.c.) shifted to the left, in salt-loaded rats and the administration of DOC produced a further increase. DOC-salt hypertension of short duration was associated with an even greater responsiveness. Sodium depletion, however, reduced responsiveness (d.r.c. shifted to the right) and concurrent DOC administration did not alter this. Angiotensin II responses were closely correlated with plasma renin concentration over a wide range of values (p.r.c, r = -0.77, P < 0.001). The differences between the groups could be explained therefore by the number of unoccupied angiotensin II receptors available.4. On the other hand only sodium loaded rats that were also receiving DOC showed any change in noradrenaline responsiveness, when the dose-response curve was shifted to the left. Noradrenaline responses showed no linear relationship to plasma renin concentration.5. The presence of hypertension did not significantly alter noradrenaline responses and the increase observed in angiotensin II responsiveness could be explained by the greater suppression of plasma renin in this group. Duration of hypertension had no effect on responsiveness to either agent.6. These results point to important differences in the pressor responsiveness to angiotensin II and noradrenaline with variation of salt intake and DOC administration.