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Lead
University of Alabama at Birmingham
Refractory hypertension refers to high blood pressure that is failing conventional antihypertensive therapies. In a retrospective assessment of such patients in our clinic we observed that resting clinic heart rates were higher in patients with refractory hypertension compared to patients with controlled hypertension. This observation has led to the hypothesis that refractory hypertension is caused by excessive sympathetic output. This protocol is designed to test this hypothesis by comparing the BP response to carvedilol verses chlorthalidone in patients with refractory hypertension. If their extreme treatment resistance is neurogenic is etiology, a significantly larger BP response to carvedilol should occur compared to chlorthalidone.
Age
19–70
Sex
ALL
Healthy volunteers
Not accepted
You may be eligible if
Uncontrolled clinic BP (\>140/90 mmHg)
Receiving 5 or more antihypertensive agents including an ACE inhibitor or ARB, calcium channel blocker, and chlorthalidone 25 mg
You may not be if
Current use of an alpha or beta or combined alpha-beta antagonist
Known allergy to alpha-beta antagonists
CKD (eGFR \<40 ml/min/m2)
MI, stroke or episode of CHF exacerbation within 3 months
Bradycardia \<50 bpm; history of 2nd or 3rd degree heart block unless treated by a pacemaker
Pregnant or breast-feeding women
Known hypersensitivity to chlorthalidone or other sulfonamide-derived drugs
Clareo Health | Mechanisms of Refractory Hypertension (Carvedilol)
