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| - Role of Presynaptic β2-Adrenergic Facilitation in the Development and Maintenance of DOCA-Salt Hypertension
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| - The present study evaluated the contribution of the presynaptic β2-adrenergic facilitation in the increase of plasma norepinephrine levels observed in deoxycorticosterone acetate (DOCA)-salt hypertension. Epinephrine is thought to be the major endogenous activator of this presynaptic mechanism and although basal epinephrine levels were similar in normotensive and DOCA-salt hypertensive rats, the sensitivity of the presynaptic β2-adrenergic facilitatory mechanism was found to be increased in hypertensive animals. This was shown in vivo by the enhanced plasma norepinephrine increases induced by a direct presynaptic stimulation with a selective β2-adrenergic receptor agonist. Furthermore, the adrenal medulla was hyperreactive in response to a hemorrhagic hypotension of 50 mm Hg, as shown by a greater plasma epinephrine increase in DOCA-salt-treated rats, and tissue concentrations of epinephrine were found to be greatly increased in the aorta of hypertensive animals. The possible contribution of epinephrine activation of the presynaptic β2-adrenergic mechanism on the development and maintenance of DOCA-salt hypertension was assessed by evaluating the effects of chronic or acute adrenalectomy, respectively. Acute adrenalectomy decreased significantly the blood pressure only in hypertensive animals, whereas chronic adrenalectomy abolished the plasma norepinephrine and blood pressure differences between normotensive and DOCA-salt-treated rats. The present results therefore suggest that the presynaptic β2-adrenergic facilitation is exaggerated in DOCA-salt hypertension, mainly due to an increased sensitivity of this mechanism and to a hyperreactivity of the adrenal medulla. Such alterations in this presynaptic facilitatory mechanism could contribute to an increase in circulating norepinephrine levels, which have been associated with the blood pressure elevation in this experimental model of hypertension. Am J Hypertens 1993;6:1016-1024
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