The effect of clonidine on human isolated smooth muscle

Coupar, Ian M.; Kirby, Marilyn J.

doi:10.1016/0014-2999(72)90268-3

Cited by 19 publications

(14 citation statements)

References 15 publications

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“…and i.c.m. clonidine, although a peripheral ci-adrenoceptor blocking action of clonidine in veins cannot be ruled out (Coupar & Kirby, 1972;Hepburn & Bentley, 1982 it produced a greater reduction in IVC blood flow as compared with i.c.m. injection, for reasons which are not immediately obvious.…”

Section: Discussionmentioning

confidence: 96%

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The effect of clonidine on venous haemodynamics in cats and dogs

Bentley

Cullen

Reynoldson

et al. 1986

British J Pharmacology

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Experiments were undertaken to investigate a possible action of clonidine on venous haemodynamics, using cats and dogs with autoperfused hindquarters. This provided an arterial input to the region independent of cardiac output. Venous capacitance in the hindquarters was indicated by blood flow in the abdominal vena cava, as measured by an electromagnetic flow probe around this vessel. It was found that in both cats and dogs, clonidine given intravenously (5 μg kg−1 i.v.) or into the cisterna magna (1 μg kg−1 i.c.m.) reduced mean arterial pressure and heart rate, but did not decrease hindquarter perfusion pressure. With the exception of dogs given i.v. clonidine, this drug caused a decrease in inferior vena cava (IVC) blood flow and this closely paralleled the hypotensive effect. However, when clonidine was given i.v. to dogs, the decrease in IVC blood flow preceded the hypotension. At the doses used, the reduction in IVC blood flow was larger following i.v. than i.c.m. clonidine in both species, and in all cases, it remained below control levels for at least 30 min, in spite of the constant arterial input to the region. In cats, dose‐response curves were constructed to noradrenaline and adrenaline given into the perfusion circuit (i.a.) before and after clonidine. Following i.v. and i.c.m. clonidine, there was a selective depression of the venoconstrictor actions of the catecholamines, but no change in the arterial pressor action. Radiographic and latex studies in the dog and cat respectively were performed in order to visualize collateral blood flow that could account for the persistent decreases in IVC blood flow. In both species, intraspinal collateral flows were demonstrated which returned blood to the heart after ligation of the inferior vena cava below the renal veins. However, it was not possible to demonstrate radiographically any changes produced by clonidine in the collateral flow because of technical difficulties. These results suggest that clonidine causes a selective reduction in sympathetic tone to the veins that is mediated at least partly by a central action, as well as an expansion of the collateral venous routes. This, together with the selective impairment of venoconstrictor responses to both noradrenaline and adrenaline, may account for the decrease in cardiac output that is most often reported following clonidine.

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Section: Discussionmentioning

confidence: 96%

“…Differences between the effects of the two injection routes were probably due to local actions of clonidine after i.v. administration, such as an a-adrenoceptor blocking action of clonidine to decrease tonic venoconstriction (Coupar & Kirby, 1972). In addition, it is possible that i.v.…”

Section: Discussionmentioning

confidence: 99%

The effect of clonidine on venous haemodynamics in cats and dogs

Bentley

Cullen

Reynoldson

et al. 1986

British J Pharmacology

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“…The functional properties of human arter ies have been studied in a number of pharma cological investigations on isolated vessels [Birmingham et al, 1969;Ettinger et al, 1970;Coupar and Kirby, 1972;Horwitz et al, 1974;Wyse, 1975;Holmberg et al, 1976;Mikkelsen et al, 1978Mikkelsen et al, , 1979, but in all these studies the vessel diameter has been larger than 0.5 mm. Morphological studies of hu man arteries have been largely confined to investigations of their cellular struc ture [Rhodin, 1962[Rhodin, , 1967, and there is little quantitative information concerning the di mensions of human resistance vessels and vascular smooth muscle cells.…”

Section: Introductionmentioning

confidence: 99%

Functional and Morphological Properties of Human Omental Resistance Vessels

Aalkjær¹,

Mulvany²

1981

J Vasc Res

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We have examined the functional and morphological properties of arterial resistance vessels with lumen diameters about 200 µm from the human omentum. The vascular smooth muscle cells were circumferentially oriented and arranged in about 3 layers within the media. The cells, when held at a length where their contractile response was maximal, were 97 µm long and had a mean diameter of 3.9 µm. In response to maximum potassium stimulation the force developed per cell was 2.4 µN. The maximum response to norepinephrine (NE) was about 90% of the response to potassium, while the sensitivity to NE (NE-ED₅₀ = 0.4 µM) was about the same as the NE sensitivity reported for larger human vessels. The sensitivity to NE was unaffected by cocaine, while the response to potassium was unaffected by phentolamine. Fluorescence microscopy indicated that the vessels contained few adrenergic nerve terminals. These findings suggest that although the vessels are well supplied with alpha-receptors, the vessels are only of minor importance for sympathetic blood pressure control.

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“…This drug also exhibits a variety of peripheral interactions with catecholamines, e.g. xlor 12-adrenoceptor stimulation (Starke & Altmann, 1973;Langer, 1977), ax-adrenoceptor blockade (Coupar & Kirby, 1972;Eltze, 1979;Ress, Field, Lockley & Fregly, 1979) and inhibition of extraneuronal amine uptake (Salt, 1972). In addition, Stone & Taylor (1978a,b) have postulated that clonidine may be an anti-adenosine agent because of its reversal of a central neuronal inhibitory response to adenosine.…”

Section: Discussionmentioning

confidence: 99%

Facilitation by Clonidine of Purine Release Induced by High Kc1 From the Rabbit Pulmonary Artery

Katsuragi

1981

British J Pharmacology

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The effect of clonidine on the 3H‐purine release evoked by KC1 or (−)‐adrenaline was assessed in the superfused helical strip of the rabbit pulmonary artery pretreated with [3H]‐adenosine. Clonidine (3 × 10−5 M to 10−4 m) significantly enhanced the 3H‐purine efflux evoked by 50 mM KC1 but not by 3 × 10−6M (−)‐adrenaline. This facilitatory effect of clonidine on the KCl‐induced purine release was unaltered by phentolamine 3 × 10−6M. It was absent in arterial segments denervated with 6‐hydroxydopamine 30 jig/ml. A sustained contractile response was evoked by clonidine 3 × 10−5 M without an increase in the 3H‐purine efflux. This was significantly reduced by phentolamine 3 × 10−6 M, but not by yohimbine 10−5M or by denervation with 6‐hydroxydopamine. 5 The uptake of [3H]‐adenosine into the segments was not inhibited by clonidine 3 × 10−5 M. It is suggested that the facilitation by clonidine of the KCl‐induced purine release is due to prevention of presynaptic autoinhibition of purine release from adrenergic nerves, by an anti‐adenosine action of the drug.

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The effect of clonidine on human isolated smooth muscle

Cited by 19 publications

References 15 publications

The effect of clonidine on venous haemodynamics in cats and dogs

The effect of clonidine on venous haemodynamics in cats and dogs

Functional and Morphological Properties of Human Omental Resistance Vessels

Facilitation by Clonidine of Purine Release Induced by High Kc1 From the Rabbit Pulmonary Artery

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