Antihypertensive effects of clonidine in tetraplegic subjects devoid of central sympathetic control

C. J. Mathias, J. L. Reid, L. M.H. Wing, H. L. Frankel, N. J. Christensen

Research output: Contribution to journalMeeting Abstractpeer-review

29 Citations (Scopus)


1. The effects of 300 μg of oral clonidine on blood pressure, heart rate, plasma noradrenaline and adrenaline concentrations were studied in seven tetraplegic subjects with physiologically complete cervical spinal cord transections.

2. Clonidine did not significantly change resting blood pressure during the 8 h of the study. Resting heart rate fell. Resting plasma noradrenaline and adrenaline concentrations, when measured 2 h after clonidine, were not significantly lower.

3. Urinary bladder stimulation resulted in a marked rise in blood pressure accompanied by an elevation in plasma noradrenaline but not adrenaline. The hypertensive response to bladder stimulation was substantially reduced by clonidine, the maximum suppression occurring 2–4 h after administration of the drug. The plasma noradrenaline response to bladder stimulation, when measured 2 h after clonidine, was significantly lower than the response before clonidine. In two tetraplegic subjects with indwelling catheters the rise in intravesical pressure caused by bladder stimulation was unchanged by clonidine.

4. The pressor response to intravenous noradrenaline in two tetraplegic subjects and to intravenous phenylephrine in a further two tetraplegic subjects was unchanged by clonidine.

5. Clonidine may have additional antihypertensive effects which occur independently of actions in the brain. These effects may be exerted by an action either on sympathetic neurones in the spinal cord or on presynaptic α-adrenoreceptors in the periphery.
Original languageEnglish
Pages (from-to)425s-428s
Number of pages4
JournalClinical Science
Issue numberSUPPL. 5
Publication statusPublished - 1 Dec 1979
Externally publishedYes


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