Interaction of Clonidine and β‐Blockers

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Abstract
On the hypothesis that non-selective .beta.-blockers can antagonize or reverse the antihypertensive effect of clinidine (C), 12 hypertensive outpatients were treated with C alone and in combination with propranolol (P), atenolol (A) and prazosin (Pz). C alone (0.11 or 0.22 mg b.i.d. [twice daily]) or in combination with P (80 mg b.i.d.) did not provide normotension. Changing P to A (50 mg b.i.d.) reduced supine systolic and diastolic pressures, which now were significantly lower (P < 0.01) than during C alone. Changing A to P again caused elevated pressures. Pz (1 mg t.i.d. [3 times daily]) added to the C + P regimen lowered supine blood pressures to the levels otherwise recorded during C + A. C dose-dependently contracted rabbit aortic spiral in vitro, reaching .apprx. 50% of maximum responses to noradrenaline [norepinephrine]. Pz abolished this response. P (0.1-10 .mu.g/ml) but not A somewhat enhanced responses to high doses of C. Sotalol rather antagonized C contractions. A but not P enhances the antihypertensive action of C. No hypertensive interaction was observed.