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α 2 -adrenoceptors (AR) lower central sympathetic output and peripheral catecholamine release, thereby protecting against sympathetic hyperactivity and hypertension. Norepinephrine re-uptake–transporter effectively (NET) removes norepinephrine from the synapse. Overflow to plasma will therefore not reflect release. Here we tested if inhibition of re-uptake allowed presynaptic α 2 AR release control to be reflected as differences in norepinephrine overflow in anesthetized hypertensive spontaneously hypertensive rats (SHR) and normotensive rats (WKY). We also tested if α 2 AR modulated the experiment-induced epinephrine secretion, and a phenylephrine-induced, α 1 -adrenergic vasoconstriction. Blood pressure was recorded through a femoral artery catheter, and cardiac output by ascending aorta flow. After pre-treatment with NET inhibitor (desipramine), and/or α 2 AR antagonist (yohimbine, L-659,066) or agonist (clonidine, ST-91), we injected phenylephrine. Arterial blood was sampled 15 min later. Plasma catecholamine concentrations were not influenced by phenylephrine, and therefore reflected effects of pre-treatment. Desipramine and α 2 AR antagonist separately had little effect on norepinephrine overflow. Combined, they increased norepinephrine overflow, particularly in SHR. Clonidine, but not ST-91, reduced, and pertussis toxin increased norepinephrine overflow in SHR and epinephrine secretion in both strains. L-659,066 + clonidine (central α 2 AR-stimulation) normalized the high blood pressure, heart rate, and vascular tension in SHR. α 2 AR antagonists reduced phenylephrine-induced vasoconstriction equally in WKY and SHR. Conclusions: α 2A AR inhibition increased norepinephrine overflow only when re-uptake was blocked, and then with particular efficacy in SHR, possibly due to their high sympathetic tone. α 2A AR inhibited epinephrine secretion, particularly in SHR. α 2A AR supported α 1 AR-induced vasoconstriction equally in the two strains. α 2 AR malfunctions were therefore not detected in SHR under this basal condition.

Plasma Norepinephrine in Hypertensive Rats Reflects α2-Adrenoceptor Release Control Only When Re-Uptake is Inhibited