Peripheral Vascular Effects of Noradrenaline, Isopropylnoradrenaline and Dopamine

Allwood, M. J.; Cobbold, A. F.; Ginsburg, Jean

doi:10.1093/oxfordjournals.bmb.a070031

Cited by 105 publications

(34 citation statements)

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“…Although the dorsal pedal artery gives off branches to the lumbrical and interosseus muscles, it supplies primarily the pads of the hind paws (Miller, Christensen & Evans, 1964). Despite an early report that the vascular bed of the hairy skin of the dog leg responded to isoprenaline almost as much as did that of skeletal muscle (Walters, Cooper, Denison & Green, 1955), it is widely assumed that fl-adrenoceptors are rare or absent in the cutaneous circulation (see, for instance, Furchgott, 1955;Skinner & Whelan, 1962;Allwood et al, 1963;Mellander & Johansson, 1968). We were therefore interested to observe that the responsiveness of the paw circulation to isoprenaline, as judged by the ratio of isoprenaline and glyceryl trinitrate responses, was more involved in control of regional resistance than is generally recognized.…”

Section: Discussionmentioning

confidence: 99%

“…As well, dopamine activates vascular a-adrenoceptors, with resultant vasoconstriction (Hamet, 1931; Allwood, Cobbold & Ginsburg, 1963;Eble, 1964;McNay & Goldberg, 1966). In the renal vasculature the density of the two receptor populations is such that local injection of dopamine in anaesthetized animals causes a net vasodilatation (Eble, 1964;McNay & Goldberg, 1966;.…”

Section: Introductionmentioning

confidence: 99%

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Localization of Vasodilator Dopamine Receptors in the Canine Hindlimb

Bell

Stubbs

1978

British J Pharmacology

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1 Vascular responses to local injection of dopamine and isoprenaline have been compared in the blood-perfused gracilis muscle and hind paw pads of dogs anaesthetized with chloralose.2 In the paw pads, dopamine (0.5 to 5.0 gg) caused a transient vasoconstriction followed by dosedependent vasodilatation. a-Adrenoceptor blockade converted this response to pure vasodilatation, which was attenuated or abolished by the dopamine-receptor antagonist, haloperidol (1 to 2mg i.a.). In the gracilis, dopamine produced only vasoconstriction. Following a-adrenoceptor blockade this was abolished, but only a very small dilator response was revealed. 3 Isoprenaline (0.05 to 0.5 jig) caused dose-dependent dilatation in both beds, which was attenuated by propranolol (0.1 mg/kg i.v.).4 Glyceryl trinitrate (0.2 to 5.0 gg) was used to assess vascular reactivity. When responses to isoprenaline and dopamine were compared with those to glvceryl trinitrate, both beds had approximately equal reactivity to isoprenaline. In contrast the paw pads were 10 fold more responsive to dopamine than was the gracilis. 5 We conclude that the vessels of the paw pads play an important part in the femoral dilator response to dopamine.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Localization of Vasodilator Dopamine Receptors in the Canine Hindlimb

Bell

Stubbs

1978

British J Pharmacology

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“…Carlsson (50) reported that there was a higher concentration of dopamine than norepinephrine in the corpus striatum and postulated that the amine may be involved in extrapyramidal function. More recently, Allwood, Cobbold, and Ginsburg (51) found that injection of dopamine into the brachial artery produced piloerection. Since a similar effect did not occur with epinephrine or norepinephrine, they suggested that dopamine may be involved in normal piloerector responses.…”

Section: Discussionmentioning

confidence: 99%

Effects of Dopamine in Man: Augmentation of Sodium Excretion, Glomerular Filtration Rate, and Renal Plasma Flow*

McDonald¹,

Goldberg²,

McNay³

et al. 1964

J. Clin. Invest.

485

148

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Dopamine (3,4-dihydroxyphenylethylamine) is considered to be the immediate metabolic precursor of norepinephrine (1), from which it differs by the absence of a P-OH group. Despite this chemical similarity, previous studies of the action of dopamine (2-9) have demonstrated that many of the circulatory and metabolic effects of this catecholamine are different from those produced by norepinephrine. Horwitz, Fox, and Goldberg (6) observed that intravenous administration of dopamine to normal subjects produced consistent increases in cardiac output and either decreased or did not change peripheral resistance. Norepinephrine, on the other hand, decreases or does not change cardiac output and increases peripheral resistance in normal subjects (10). The circulatory effects of dopamine are potentiated by monoamine oxidase inhibitors to a much greater extent than are those of norepinephrine (9). Dopamine also contrasts with norepinephrine in its failure to increase circulating free fatty acids (7,8). These differences suggest that the effects of

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“…Norepinephrine is the major neurotransmitter in the peripheral sympathetic nervous system, whereas epinephrine is the primary hormone secreted by the adrenal medulla in mammals (2).…”

Section: Introductionmentioning

confidence: 99%

Catecholamine-induced vasoconstriction is sensitive to carbonic anhydrase I activation

Puşcaş¹,

Coltâu²,

Gilau³

et al. 2001

Braz J Med Biol Res

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We studied the relationship between alpha-and beta-adrenergic agonists and the activity of carbonic anhydrase I and II in erythrocyte, clinical and vessel studies. Kinetic studies were performed. Adrenergic agonists increased erythrocyte carbonic anhydrase as follows: adrenaline by 75%, noradrenaline by 68%, isoprenaline by 55%, and orciprenaline by 62%. The kinetic data indicated a non-competitive mechanism of action. In clinical studies carbonic anhydrase I from erythrocytes increased by 87% after noradrenaline administration, by 71% after orciprenaline and by 82% after isoprenaline. The increase in carbonic anhydrase I paralleled the increase in blood pressure. Similar results were obtained in vessel studies on piglet vascular smooth muscle. We believe that adrenergic agonists may have a dual mechanism of action: the first one consists of a catecholamine action on its receptor with the formation of a stimulus-receptor complex. The second mechanism proposed completes the first one. By this second component of the mechanism, the same stimulus directly acts on the carbonic anhydrase I isozyme (that might be functionally coupled with adrenergic receptors), so that its activation ensures an adequate pH for stimulus-receptor coupling for signal transduction into the cell, resulting in vasoconstriction. Correspondence

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Peripheral Vascular Effects of Noradrenaline, Isopropylnoradrenaline and Dopamine

Cited by 105 publications

References 0 publications

Localization of Vasodilator Dopamine Receptors in the Canine Hindlimb

Localization of Vasodilator Dopamine Receptors in the Canine Hindlimb

Effects of Dopamine in Man: Augmentation of Sodium Excretion, Glomerular Filtration Rate, and Renal Plasma Flow*

Catecholamine-induced vasoconstriction is sensitive to carbonic anhydrase I activation

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