Circulatory Effects at Rest and Exercise of Clonidine, an Imidazoline Derivative With Hypotensive Properties

Muir, Alexander; Burton, Jeff; Lawrie, D.M.

doi:10.1016/s0140-6736(69)91423-8

Cited by 57 publications

(16 citation statements)

References 12 publications

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“…In agreement with a number of previous reports (Morley et al 1991;Muzi et al 1992;Tulen et al 1992), clonidine had no significant effect on heart rate at 20 8C. Although there have been reports of bradycardia caused by clonidine (Barnett and Cantor 1968;Muir et al 1969;Fleming et al 1991), the effect of clonidine on heart rate is usually small (Reid 1981) and variable (Glue and Nutt 1988), probably reflecting the relatively low level of sympathetic drive to the hearts of resting subjects (Muzi et al 1992). However, when clonidine was applied at 40 8C it was able to antagonise the increase in heart rate evoked by high ambient temperature.…”

Section: Discussionsupporting

confidence: 88%

Comparison of the effects of high ambient temperature and clonidine on autonomic functions in man

Arya

Langley

Szabadi

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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The effects of two interventions, high ambient temperature, a sympathetic activator, and clonidine, a centrally acting sympatholytic drug, were compared on a number of autonomic functions. Eight healthy male volunteers participated in four weekly sessions. Each session was associated with one of the following treatments: placebo (physiological saline infused intravenously over 10 min) at 20 degrees C; clonidine hydrochloride (1.5 micrograms kg-1 in 10 ml infused intravenously over 10 min) at 20 degrees C; placebo at 40 degrees C; clonidine at 40 degrees C. Subjects were allocated to treatments and sessions according to a double-blind (for drug condition) balanced design. In each session, the following indices of autonomic function were recorded: systolic and diastolic blood pressure, heart rate, salivation, body temperature, plasma noradrenaline and adrenaline concentrations, baseline and carbachol-evoked sweating, physiological finger tremor. Raised ambient temperature (40 degrees C) caused increases in heart rate, body temperature, carbachol-evoked sweating and physiological finger tremor. Clonidine (at 20 degrees C) reduced systolic blood pressure, body temperature, salivation and plasma noradrenaline concentration, but did not affect any of the other measures. Clonidine (at 40 degrees C) counteracted the increase in heart rate, but not the increases in carbachol-evoked sweating and finger tremor, evoked by high ambient temperature. The high ambient temperature condition abolished the body-temperature-lowering effect of clonidine, but did not modify the effects of clonidine on systolic blood pressure, salivation and plasma noradrenaline concentration. These result indicate that while the effects of the heat stressor are consistent with an increase in sympathetic activity, and most of the effects of clonidine are consistent with a decrease in sympathetic activity, only two functions (body temperature and heart rate) were affected in opposite directions by the two interventions. Indeed physiological antagonism between the two interventions could be demonstrated on body temperature and heart rate only, and there was no evidence for an interaction between the effects of the two variables on any of the other indices of autonomic activity. The failure of clonidine to affect two sympathetically mediated functions, carbachol-evoked sweating and physiological finger tremor, under either temperature condition, indicates that central alpha 2-adrenoceptors cannot be involved in the regulation of these functions.

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Section: Discussionsupporting

confidence: 88%

Comparison of the effects of high ambient temperature and clonidine on autonomic functions in man

Arya

Langley

Szabadi

et al. 1997

Naunyn-Schmiedeberg's Arch Pharmacol

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“…As shown in figure 2, the changes in blood pres sure after acute administration of both drugs in normal volunteers were not even nominally significant at the 5% level, although guanfacine seemed to exert less of a hypotensive effect than clonidine over 8 h. However, clinical long-term guanfacine studies suggest that blood pressure is brought under control and stabilized at a nonpathological level within about 2 weeks [35]. And the decrease reached statistical significance in week 3 for systolic blood pressure and week 4 for diastolic blood pressure [22], while chronic treatment with clon idine has been reported to reduce blood pressure by less than it falls after a single dose [21,23,24]. This acute study did not produce any clear evidence regarding the relative superiority of the antihypertensive effect of the two drugs.…”

Section: Discussionmentioning

confidence: 99%

Electroencephalographic and Psychometric Assessment of the CNS Effects of Single Doses of Guanfacine Hydrochloride (Estulic®) and Clonidine (Catapres®)

Yamadera

Ferber²,

Matejcek³

et al. 1985

Neuropsychobiology

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A double-blind, placebo-controlled study was carried out in 10 young healthy volunteers to investigate the effects of single doses of 1 and 2 mg guanfacine hydrochloride (Estulic®) and 0.15 and 0.3 mg clonidine (Catapres®) on the electroencephalogram (EEG), subjective mental and emotional state, blood pressure and heart rate. These doses are considered to be equipotent with regard to their antihypertensive effects, as shown in long-term therapeutic trials. Each subject received all five treatments in random sequence at intervals of 1 week. The EEG tracings were evaluated quantitatively by spectral analysis. Procedures were carried out before and at 1, 2, 4, 6 and 8 h after drug administration. After clonidine the EEG showed increased slow-wave activity and decreased alpha activity, these effects being dose-dependent. They were of the sedative type and did not clearly indicate specific psychotropic properties. The subjective mental and emotional state questionnaire indicated a decrease of alertness, extroversion, concentration and mood (in that order), changes which paralleled the EEG changes. The changes observed after guanfacine were qualitatively similar to those after clonidine, but were of considerably lower intensity. Our data suggest that guanfacine has less central nervous system-depressant activity than clonidine.

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“…We have observed significant falls in pressure not only in essential hypertensives but also in normal subjects ( Figure 2) . The fall in pressure which is usually accompanied by a modest bradycardia appears to result from a fall in peripheral resistance and an additional but variable fall in cardiac output (Muir, Burton & Lawrie, 1969;Barnett & Cantor, 1968). After 300 ,ug orally, the fall in blood pressure is apparent by 1 h, maximal between 2 and 4 h and recovery takes place over 8-12 h. The fall in blood pressure after intravenous clonidine 300 ,ug was of similar magnitude and although the pressure fell within minutes of dosing the maximum fall was not observed for 1-2 h (Davies et al, 1977).…”

Section: Clinical Pharmacodynamics Of Clonidinementioning

confidence: 99%

The Fourth Lilly Prize Lecture, University of Aberdeen, September 1980. The clinical pharmacology of clonidine and related central antihypertensive agents.

Reid¹

1981

Brit J Clinical Pharma

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Circulatory Effects at Rest and Exercise of Clonidine, an Imidazoline Derivative With Hypotensive Properties

Cited by 57 publications

References 12 publications

Comparison of the effects of high ambient temperature and clonidine on autonomic functions in man

Comparison of the effects of high ambient temperature and clonidine on autonomic functions in man

Electroencephalographic and Psychometric Assessment of the CNS Effects of Single Doses of Guanfacine Hydrochloride (Estulic®) and Clonidine (Catapres®)

The Fourth Lilly Prize Lecture, University of Aberdeen, September 1980. The clinical pharmacology of clonidine and related central antihypertensive agents.

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