Plasma adrenaline modulates al1-adrenoceptor mediated pressor responses and the baroreflex control in patients with borderline hypertension

Plasma level of adrenaline has been reported to be elevated in borderline hypertension. However, its role in developing and maintaining hypertension is still not completely understood. This study aimed to estimate the role of plasma adrenaline in developing hypertension. Ten patients with borderline hypertension (BHT) and 10 age-matched normotensive subjects were included. We infused at least three graded doses of phenylephrine, an aL-adrenoceptor agonist, into the antecubital vein of subjects lying quietly in a supine position. Mean blood pressure was measured continuously through the right radial artery. Cardiac output was measured by the thermodilution method before and after the administration of each dose of phenylephrine infusion. We obtained dose-response curves for mean blood pressure and total peripheral resistance to phenylephrine. Baroreflex sensitivity was calculated by plotting the longest R-R intervals against the elevated peak mean blood pressure after the infusion of each dose of phenylephrine. Plasma noradrenaline and adrenaline concentrations at rest were measured by high performance liquid chromatography coupled with trihydroxyindole fluorimetric detection. The plasma adrenaline level at rest was higher in patients with BHT than in normotensive subjects. With graded infusion of phenylephrine, both the pressor responses and the changes in total peripheral resistance were greater in patients with BHT than in normotensive subjects. The plasma adrenaline level was positively correlated with the slope of dose response curves for the increments of mean blood pressure to phenylephrine (r = 0.60, p < 0.01). Baroreflex sensitivity was reduced in patients with BHT as compared with normotensive subjects. Baroreflex sensitivity was inversely correlated with plasma adrenaline level (r = 0.749, p < 0.001). These results suggest that plasma adrenaline is involved in the initiation or maintenance of high blood pressure in BHT by enhancing aL1-adrenoceptor mediated vasoconstriction and reducing the baroreflex sensitivity.