Key result
Chronic sympatho-inhibition with rilmenidine normalized mean arterial pressure and reduced basal plasma renin activity without compromising blood flow in the stenosed kidney in 2K1C rabbits.
Why the study?
Does chronic sympatho-inhibition with rilmenidine alter responses of renal blood flow and plasma renin activity to stress and acute hypotension in rabbits with renovascular hypertension?
Does chronic sympatho-inhibition with rilmenidine alter responses of renal blood flow and plasma renin activity to stress and acute hypotension in rabbits with renovascular hypertension?
Chronic sympatho-inhibition with rilmenidine effectively normalizes blood pressure and reduces basal plasma renin activity without compromising blood flow in the stenosed kidney in a rabbit model of renovascular hypertension.
May inform sympatho-inhibition strategies in renovascular hypertension; leaves open translation to human stress or hypotensive responses.
BACKGROUND AND PURPOSE: We determined if chronic sympatho-inhibition with rilmenidine has functional significance for the kidney by altering responses of renal blood flow (RBF) and plasma renin activity (PRA) to stress and acute hypotension in rabbits with renovascular hypertension. EXPERIMENTAL APPROACH: RBF to each kidney and renal sympathetic nerve activity (RSNA) to the left kidney were measured in rabbits in which a renal artery clip induced hypertension (2K1C) and in sham-operated rabbits. After 2 weeks, a subcutaneous minipump was implanted to deliver rilmenidine (2.5 mg.kg(-1).day(-1)) to 2K1C rabbits for 3 weeks. KEY RESULTS: After 5 weeks of renal artery stenosis, mean arterial pressure (MAP) was 23% higher and PRA 3-fold greater than in sham-operated rabbits. Blood flow and renal vascular conductance in the stenosed kidney were lower (-75% and -80%) compared with sham, and higher in the non-clipped kidney (68% and 39%). Responses of RBF and PRA to hypotension were similar in 2K1C and sham rabbits. Airjet stress evoked a greater increase in MAP in 2K1C rabbits than sham controls. Chronic rilmenidine normalized MAP, reduced RSNA and PRA, and did not reduce RBF in the stenosed kidney. Responses of RBF (clipped and non-clipped kidney), RSNA and PRA to hypotension and airjet were little affected by rilmenidine. CONCLUSIONS AND IMPLICATIONS: Our observations suggest that chronic sympatho-inhibition is an effective antihypertensive therapy in renovascular hypertension. It normalizes MAP and reduces basal PRA without compromising blood flow in the stenosed kidney or altering responses of MAP, haemodynamics and PRA to acute hypotension and stress.
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Burke et al. (2009) studied Renovascular hypertension. Rilmenidine vs. Sham-operated rabbits was evaluated on Renal blood flow (RBF), plasma renin activity (PRA), mean arterial pressure (MAP), and renal sympathetic nerve activity (RSNA). Chronic sympatho-inhibition with rilmenidine normalized mean arterial pressure and reduced basal plasma renin activity without compromising blood flow in the stenosed kidney in 2K1C rabbits.
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