Plasma adrenaline responses to long-term modification of blood pressure in normotensive rats and hypertensive rats.

OBJECTIVE

To examine the relationship between plasma adrenaline and hypertension.

DESIGN

Plasma adrenaline responses to chronic manipulations of blood pressure were tested in normotensive and in hypertensive rats.

METHODS

Hypertension was induced in normotensive Wistar-Kyoto (WKY) rats by administration of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME), and blood pressure was lowered in stroke-prone spontaneously hypertensive rats (SHRSP) by administering hydralazine. Plasma catecholamine responses were monitored using blood samples from conscious unrestrained rats under resting conditions.

RESULTS

Twenty-four hours after starting L-NAME treatment, mean arterial pressure was 22 mmHg higher than in control WKY rats. Heart rate and plasma noradrenaline were reflexly reduced, but plasma adrenaline was unaffected. After 4 weeks of L-NAME treatment mean arterial pressure was 48 mmHg higher than in untreated rats. At this stage heart rate had returned to normal, but plasma noradrenaline was 33% higher and plasma adrenaline was 117% higher than in untreated rats. The elevation of plasma adrenaline was confirmed in a study of longer duration, in which plasma adrenaline had doubled after 10 weeks of L-NAME treatment. Conversely, 24 h after hydralazine treatment in SHRSP, mean arterial pressure was reduced by 49 mmHg and there was a reflex elevation of plasma adrenaline, noradrenaline and heart rate. However, after 19 days of blood pressure reduction with hydralazine, plasma noradrenaline and heart rate had returned to normal, but plasma adrenaline had fallen to 30% below normal. Most of the change in mean arterial pressure observed with either chronic L-NAME or hydralazine could be attributed to modulation of neurally mediated vasoconstriction, estimated from mean arterial pressure responses to acute autonomic blockade.

CONCLUSION

Selective changes in plasma adrenaline levels were induced by chronic experimental manipulations of blood pressure. This implies that the high plasma adrenaline level observed in spontaneously hypertensive rats might be a consequence rather than a cause of their hypertension.