Prejunctional β-adrenoceptors in human digital arteries

Stevens, M. J.; Rittinghausen, R.; Medcalf, Robert L.; Moulds, R. F. W.

doi:10.1016/0014-2999(82)90259-x

Cited by 29 publications

(14 citation statements)

References 16 publications

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“…For instance, one might speculate that the stimulation-evoked release of 'H-adrenaline consisted of a smaller and broader "'H-overflow peak" compared to a possible tall and narrow "'H-overflow peak" of 'H-noradrenaline incubated tissue. As this was not the case, the main conclusion was that 'H- Stevens et al 1982 adrenaline was released by electrical-field stimulation from rabbit isolated thoracic aorta in much the same manner as 'H-noradrenaline. For both of the 'H-amines more than 96% of the total stimulation-evoked 'H-overflow was contained in the initial 4 two-min fractions ( fig.…”

Section: Adrenaline Releasementioning

confidence: 93%

“…The effect of exogenous adrenaline on 3H-noradrenaline release by electrical-field stimulations has been studied in several cardiovascular tissues (table 5) including 12 blood vessels from 5 species. Adrenaline solely facilitated stimulation-evoked 'H-noradrenaline release by the activation of prejunctional padrenoceptors only in 4 blood vessels (Stjarne and Brundin 1975;Westfall et al 1979;Stevens et al 1982;Gothert and Kollecker 1986) and this effect was antagonized by p-…”

Section: Adrenaline Releasementioning

confidence: 98%

“…This hypothesis was based in part on the observation that exogenous adrenaline (i.e. adrenaline added to the tissue bath) in low concentration enhances the stimulation-evoked release of 3H-noradrenaline in some isolated vessels (StjHrne and Brundin 1975, Westfall et al 1979, Stevens et al 1982, Gothert and Kollecker 1986. However, in some vascular tissues, the enhancement was not seen (Hope et al 1976, Gothert and Hentrich 1985, Molderings et al 1988a).…”

Section: Introductionmentioning

confidence: 99%

“…neurogenic adrenaline) together with noradrenaline (GuimarBes et al 1978, Majewski et al 1980, 1981a, Stevens et al 1982, Molderings et al 1988a. Neurogenic adrenaline has been shown to activate prejunctional P-adrenoceptors in some tissues (Gui-marBes et al 1978, Majewski et al 1980, 1981a but not all (Stevens et al 1982, Molderings et al 1988a.…”

Section: Introductionmentioning

confidence: 99%

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Accumulation and release of adrenaline, and the modulation by adrenaline of noradrenaline release from rabbit blood vessels in vitro

Abrahamsen

1991

Pharmacology & Toxicology

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The accumulation of (-)-3H-adrenaline (3H-A) by rabbit isolated aorta was studied. In all experiments, monoamine oxidase and catechol-O-methyltransferase were inhibited by treatment with pargyline and 3',4'-dihydroxy-2-methyl-propiophenone, respectively. The relationship between the accumulation of 3H derived from 3H-A and the duration of incubation was linear. The 3H-accumulation after 3 h incubation was 22.5 ml/g. In reserpine-treated tissue, the 3H-accumulation levelled off after 30 min and was 8.5 ml/g after 3 h. The concentration of 3H-A or (-)-3H-noradrenaline (3H-NA) and the 3H-accumulation (ml/g) were inversely related. At 10(-8) M, the 1-hour accumulation of 3H derived from 3H-A and 3H-NA was 7.8 and 15.2 ml/g, respectively. With increasing concentrations the accumulation values approached each other. The accumulation of 3H derived from 3H-A by reserpine-treated tissue also showed an inverse relationship with concentration. The accumulation of 3H derived from 3H-A was dependent on the bath temperature. Storage of tissue (0-5 days in salt solution without equilibration with 95% O2/5% CO2; 4 degrees C) did not affect the accumulation of 3H derived from 3H-A. Thereafter (7-14 days), the accumulation decreased. The inhibitory potency (IC50; -log M) of desipramine, cocaine, propranolol, isoprenaline, and normetanephrine on accumulation of 3H derived from 3H-A was found to be 8.26; 6.50; 5.48; 4.88, and 4.02, respectively. The maximal degree of inhibition was almost the same for these drugs, while that of clonidine and corticosterone was 50 and 20%, respectively. In the presence of desipramine, either clonidine, corticosterone or isoprenaline reduces the accumulation of 3H derived from 3H-A. Ouabain and iodoacetic acid, but not sodium cyanide and 2,4-dinitrophenol, reduced the accumulation of 3H derived from 3H-A. Anoxia (95% N2/5% CO2; 37 degrees C; 1-24 h) did not alter the accumulation of 3H derived from 3H-A. Glucose deprivation alone or combined with anoxia markedly reduced the 3H-accumulation. The release of 3H-A from rabbit isolated aorta was studied. This release was compared with that of 3H-NA. The stimulation-evoked 3H-overflow from aorta preloaded with 3H-A decreased with repeated stimulation. In contrast, prestimulation enhanced subsequent stimulation-evoked 3H-overflows. For both 3H-amines, the 3H-overflow increased concomitantly to the same degree with the number of pulses. The time course of 3H-overflows with either 3H-A or 3H-NA was compared.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Adrenaline Releasementioning

confidence: 93%

Section: Adrenaline Releasementioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Accumulation and release of adrenaline, and the modulation by adrenaline of noradrenaline release from rabbit blood vessels in vitro

Abrahamsen

1991

Pharmacology & Toxicology

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“…This confirms findings with guinea pig pulmonary artery [23] and rat perfused kidney [24] where adrenaline solely produced an attenuation of the stimulation-evoked transmitter release. On the other hand, exogenously applied adrenaline enhanced the stimulation-evoked 3H overflow in rat portal vein [25], human omental blood vessels [20] and human dig ital arteries [26].…”

Section: Discussionmentioning

confidence: 99%

Presynaptic Modulation by Adrenaline of <sup>3</sup>H-Noradrenaline Release in Rabbit Ear Artery

Abrahamsen¹,

Nedergaard²

1991

Pharmacology

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The aim of the present investigation was to examine the ability of adrenaline to modulate presynaptically the stimulation-evoked release of noradrenaline from postganglionic sympathetic nerves in the rabbit ear artery. Strips of rabbit central ear artery were incubated with ³H-noradrenaline. Subsequently, they were washed repeatedly with physiological salt solution containing cocaine and corticosterone. The strips were subjected to repeated electrical-field stimulation (S₁–S₈, 150 pulses, 0.5 ms, 225 mA, 3 Hz) and the resultant ³H overflow was determined. Adrenaline (10^–8 to 10^–6 mol/l) and clonidine (10^–9 to 10^–6 mol/l) reduced the stimulation-evoked 3H overflow. Rauwolscine (10^–7 to 10^–5 mol/l) and phentolamine (3 × 10^–7 to 3 × 10^–5 mol/l) enhanced markedly the stimulation-evoked 3H overflow. Rauwolscine (10^–6 mol/l) abolished the inhibitory effect of low concentrations of adrenaline (10^–8 to 10^–7 mol/l) and clonidine (10^–9 to 10^–7 mol/l) and attenuated the inhibitory effect of the highest concentration (10^–6 mol/l) of clonidine, but not that of adrenaline. In some experiments, the stimulation current was reduced to 175 mA in order to obtain similar reference release (S₃) values despite the presence of rauwolscine. Even then, only the highest concentration (10^–6 mol/l) of adrenaline decreased the stimulation-evoked ³H overflow. Facilitation was not seen. It is concluded that adrenaline activates inhibitory presynaptic α₂-adrenoceptors. Furthermore, adrenaline does not reveal the presence of presynaptic facilitatory β-adrenoceptors in the rabbit ear artery.

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Presynaptic β‐adrenoceptors

Misu

Kubo

1986

Medicinal Research Reviews

115

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The existence of facilitatory presynaptic beta-adrenoceptors has been shown in approximately 30 tissues of 6 different species including human. A positive feed back loop for further release of the transmitter appears to be activated by an endogenous agonist, epinephrine, taken up and released as a cotransmitter with norepinephrine rather than norepinephrine itself released from peripheral noradrenergic nerve terminals. Presynaptic beta-adrenoceptors are mainly of a beta 2-subtype. Some beta 1-subtype receptors are also suggested. There coexist presynaptic beta 1- and beta 2-adrenoceptors in cat and rat hypothalamus. Higher sensitivity of peripheral presynaptic beta-adrenoceptors to isoproterenol may be implicated in the early development of hypertension in SHR. Epinephrine taken up and released initiates the development of hypertension in rats via activation of these receptors. Increased activation of these receptors by epinephrine may play a role in the development of essential hypertension. The antihypertensive action of beta-antagonists may be in part due to blockade of these facilitatory presynaptic beta-adrenoceptors.

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Prejunctional β-adrenoceptors in human digital arteries

Cited by 29 publications

References 16 publications

Accumulation and release of adrenaline, and the modulation by adrenaline of noradrenaline release from rabbit blood vessels in vitro

Accumulation and release of adrenaline, and the modulation by adrenaline of noradrenaline release from rabbit blood vessels in vitro

Presynaptic Modulation by Adrenaline of <sup>3</sup>H-Noradrenaline Release in Rabbit Ear Artery

Presynaptic β‐adrenoceptors

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