Why the study?
Does clonidine treatment affect cardiopulmonary baroreflex induced sympathetic activation in older patients with mild-to-moderate hypertension?
Does clonidine treatment affect cardiopulmonary baroreflex induced sympathetic activation in older patients with mild-to-moderate hypertension?
Low-dose clonidine lowers peripheral vascular resistance and alters responses to cardiopulmonary baroreceptor unloading in older hypertensive patients, suggesting peripheral mechanisms of action.
May support low-dose clonidine for vascular effects in older hypertensives; leaves open baroreflex modulation pending randomized confirmation.
Summary: To determine whether clonidine treatment affects cardiopulmonary baroreflex induced sympathetic activation, we assessed the hemodynamic and hormonal responses to lower body negative pressure (LBNP) before and after 3 weeks of treatment with low-dose (0.2 mg daily) clonidine in eight older (mean age, 62 years) patients with established mild-to-moderate hypertension. Arterial pressure, heart rate (HR), forearm vascular resistance (FVR), plasma norepinephrine (NE), and renin activity (PRA) responses were assessed. Our results demonstrate that clonidine treatment had no effect on basal or stimulated PRA and plasma NE levels at baseline and during LBNP. Baseline FVR significantly decreased (48 ± 3 to 35.5 ± 6 U) and the FVR responses to LBNP were lower following clonidine therapy. Although baseline mean arterial pressure (MAP) and FVR as well as FVR responses to LBNP were lower after clonidine, the responses to tilt and cold pressor testing were unchanged. Thus clonidine appears to act via peripheral mechanisms, as well as by decreasing central sympathetic outflow to lower peripheral vascular resistance.
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Mohanty et al. (1987) studied this question.
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