Indirect adrenergic effect of histamine in cat cerebral arteries

Marco, E.; Balfagón, Gloria; Marı́n, Jesús; Gómez, B.; Lluch, Salvador

doi:10.1007/bf00499153

Cited by 20 publications

(2 citation statements)

References 13 publications

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“…Indeed, histamine triggers noradren- aline release in cat (Marco et al 1980;Balfagon et al 1984) and human cerebral arteries. Moreover, phentolamine and other a-adrenoceptor antagonists reportedly inhibit the contracting effect of histamine in some isolated blood vessels, including the cerebral arteries of the cat (Marco et al 1980) and the portal veins of the rabbit (Cook & MacLeod 1978;MacLeod et al 1980) and of the dog (Bielkiewicz & Cook 1984). However, phentolamine (0.3 pM) did not antagonize histamine-induced contractions either in HSV or in HIMA, ruling out the involvement of a catecholamine-releasing effect of histamine in these vessels.…”

Section: Discussionmentioning

confidence: 99%

Histamine Receptors in the Smooth Muscle of Human Internal Mammary Artery and Saphenous Vein

Schoeffter

Godfraind

1989

Pharmacology & Toxicology

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The effects of histamine were characterized and compared in the vascular smooth muscle of two human isolated blood vessels, the human internal mammary artery (HIMA) and the human saphenous vein (HSV). Segments of these vessels were obtained during aortocoronary bypass surgery and their intimal surface was rubbed in order to eliminate any possible influence of the endothelium. Histamine contracted both types of vessels in a concentration-dependent manner and this effect was antagonized by the H1 receptor antagonists mepyramine and cicletanine. In the case of HIMA only this antagonism was found to be competitive (pA2 values of 9.3 and 7.7 for mepyramine and cicletanine, respectively). Histamine-induced contractions were not significantly affected by phentolamine (0.3 microM). In HSV, but not HIMA, indomethacin (5 microM) significantly depressed histamine-induced contractions (by about 30%). In the presence of the H2 receptor antagonist cimetidine (10 microM), concentration-response curves of histamine-induced contractions were significantly shifted to the left in both HIMA and HSV, suggesting the presence of H2 receptors mediating relaxation. HIMA and HSV precontracted by noradrenaline could be partially and concentration dependently relaxed by histamine, only in the presence of a H1 receptor antagonist. This relaxation was inhibited by cimetidine. The results show that in de-endothelialized HIMA and HSV histamine induced mainly contraction which is sensitive to the H1 receptor antagonists. Only in HIMA, nevertheless, was competitive antagonism established. In addition, histamine-induced relaxation, antagonized by cimetidine, could be demonstrated in both precontracted vessels, indicating the presence of H2 receptors.

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Section: Discussionmentioning

confidence: 99%

Histamine Receptors in the Smooth Muscle of Human Internal Mammary Artery and Saphenous Vein

Schoeffter

Godfraind

1989

Pharmacology & Toxicology

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“…After this incubation period the arteries were transferred into a superfusion chamber to study the release of radioactivity according to Farnebo & Malmfors (1971) as described by Marco et al (1980). 5 4 kg, were anaesthetized with sodium pentobarbitone (35 mg kg-1 i.p.)…”

Section: A T E R I a L S A N D Methodsmentioning

confidence: 99%

Mechanism of the indirect adrenergic effect of histamine in cat cerebral arteries

Balfagón

Galván

Marco

1984

Journal of Pharmacy and Pharmacology

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KCl (50 mM), tyramine (10(-7) M), and histamine (10(-4) M) induced an increase in tritium release from cat cerebral arteries preincubated with [3H]noradrenaline, this increase being due in part to noradrenaline. When calcium was absent from the superfusion medium, only tyramine (10(-7) M) enhanced the tritium outflow. Colchicine (10(-3) M) partially inhibited the increase in radioactivity brought about by 10(-4) M histamine. KCl (50 mM) also evoked release of radioactivity from cerebral arteries preloaded with [3H]histamine; this release was unaffected by reserpine pretreatment or removal of both superior cervical sympathetic ganglia. Neither tyramine (10(-7) M) nor compound 48/80 (300 micrograms ml-1) altered the spontaneous tritium outflow from cerebral blood vessels preincubated with [3H]histamine. These results suggest that histamine is not accumulated by sympathetic nerve endings and elicits its noradrenaline-releasing effect by means of an exocytotic process.

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In vivo release by histamine agonists and antagonists of endogenous catecholamines in the cat hypothalamus

Philippu

Bald

Kraus

et al. 1984

Naunyn-Schmiedeberg's Arch. Pharmacol.

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The posterior hypothalamus of anaesthetized cats was superfused through a push-pull cannula with histamine agonists and antagonists and the release of endogenous catecholamines was determined in the superfusate. Hypothalamic superfusion with histamine, 2-methylhistamine (H1-agonist), dimaprit (H2-agonist) or metiamide (H2-antagonist) enhanced the release of the catecholamines dopamine, noradrenaline and adrenaline. The releasing effects of these substances depended on the presence of calcium ions. Superfusion with 2-pyridylethylamine (H1-agonist) was virtually ineffective, while superfusion with 2-thiazolethylamine (H1-agonist) enhanced the rates of release of noradrenaline and adrenaline without influencing the release of dopamine. Superfusion with mepyramine (H1-antagonist) inhibited the release of noradrenaline and adrenaline without affecting the release of dopamine. Hypothalamic superfusion with a concentration of procaine which was equi-anaesthetic to that of mepyramine was ineffective. Ranitidine (H2-antagonist) did not alter the rates of release of the catecholamines. The releasing effect of histamine was inhibited on hypothalamic superfusion with mepyramine and ranitidine. Ranitidine also inhibited the releasing effects of dimaprit and 2-methylhistamine thus indicating that the releasing action of the latter compound was mainly due to stimulation of H2-receptors. These data suggest that blockade of H1-receptors of the posterior hypothalamus reduces the release of noradrenaline and adrenaline, while stimulation of H1-receptors seems to increase the rates of release of these two catecholamines. Stimulation of H2-receptors enhances the release of all three catecholamines. Thus, dopaminergic neurones of the hypothalamus seem to possess H2-receptors, while noradrenergic and adrenergic neurones possess H1- and H2-receptors.

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Indirect adrenergic effect of histamine in cat cerebral arteries

Cited by 20 publications

References 13 publications

Histamine Receptors in the Smooth Muscle of Human Internal Mammary Artery and Saphenous Vein

Histamine Receptors in the Smooth Muscle of Human Internal Mammary Artery and Saphenous Vein

Mechanism of the indirect adrenergic effect of histamine in cat cerebral arteries

In vivo release by histamine agonists and antagonists of endogenous catecholamines in the cat hypothalamus

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