Regulation of catecholamine release by presynaptic receptor system

Patel, Saket; Patel, Umesh; Vithalani, Dinesh; Verma, S. C.

doi:10.1016/0306-3623(81)90063-x

Cited by 29 publications

(4 citation statements)

References 114 publications

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“…The kidney was removed from the animal and perfused at a rate of 6 ml/min with Krebs-Ringer bicarbonate solution. After a stabilization period of 20 to 30 minutes, the neuronal norepinephrine storage sites were labelled with € [7,8 3 H]-norepinephrine ( 3 H-NE). Then 10 /xCi 3 H-NE (11 Ci/mmoles) was perfused through the kidney for 30 minutes followed by a 40-minute washout with 3 H-NE free fluid.…”

Section: Methodsmentioning

confidence: 99%

“…5 - 6 Norepinephrine released during nerve activity can cause an inhibition of further transmitter release by activating presynaptic a-adrenoceptors, which is an important negative feedback mechanism involved in the modulation of neurotransmitter release. 7 - 8 Although a physiological role of presynaptic /3-adrenoceptors has not yet been demonstrated, it has been shown that these receptors may be the target sites for circulating epinephrine. 5 -9 Involvement of the sympathetic nervous system in the pathogenesis of hypertension in spontaneously hypertensive rats (SHR) has been extensively studied.…”

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confidence: 99%

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Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Ekas¹,

Steenberg²,

Woods³

et al. 1983

Hypertension

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SUMMARY The present study was designed to measure norepinephrine release during sympathetic nerve stimulation and evaluate the presynaptic inhibitory and facilitatory actions of a-adrenoceptor and /3-adrenoceptor agonists respectively, in the isolated perfused kidney of normotensive WistarKyoto (WKY) and spontaneously hypertensive rats (SHR). Periarterial nerve stimulation (0.25 to 32 Hz) caused a significantly greater release of norepinephrine, which was measured as total tritium overflow, in the SHR. The vasoconstrictor responses to periarterial nerve stimulation as well as to norepinephrine, angiotensin II, and barium chloride were also significantly greater in the SHR. Presynaptic actions of tramazoltne, an a 2 -adrenoceptor agonist, and salbutamol, a /3 2 -adrenoceptor agonist, on norepinephrine release were determined during periarterial nerve stimulation at 2 Hz.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Ekas¹,

Steenberg²,

Woods³

et al. 1983

Hypertension

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“…Data not given Spectrophotofluorimetrically determined Liver, kidney, spleen, skeletal muscle, brain Colorimetric determination including adrenaline and "adrenaline-like'' material (AC = adsorbable chromogens) Heart, liver, kidney, intestine, lung, skeletal muscle, skin, urine, plasma, blood cells, expired carbondioxide, site of injection Pithed animal Estimated weights: rat = 300 g, cat = 3 kg Biological assay to distinguish adrenaline from noradrenaline Liver, kidney, intestine, heart, lung, fetal placenta, brain Io-'g/fetus Spleen, kidney, intestine, skeletal muscle, skin Adrenal glands were removed Dose per minute, no exact infusion time was given Heart, spleen, liver, kidney, skeletal muscle Heart, spleen, lung, liver, small intestine, skeletal muscle, kidney, adrenal gland, pituitary gland, brain, salivary gland, pancreas, plasma Liver, skeletal muscle, 8 brain areas Abstract Heart, liver, kidneys, spleen, lungs, skeletal muscle, diaphragm, stomach, jejunum, peritoneal fat, brain, urine, blood External ocular muscle, retractor bulbi muscle, lacrimal gland, salivary gland Skeletal muscle, liver, pineal body, plasma, cerebrospinal fluid, 9 brain areas Aorta, renal arteries, vena cava inferior Removal determined as arterio-venous difference, accumulation as adrenal content in femoral artery and saphenous vein 1976; Starke et al 1975aStarke et al , 1977Starke et al , 1989Kirpekar 1974/75;Stjarne 1975;Bacq 1976;Westfall 1977Westfall , 1980Vizi 1979;Gillespie 1980;Rand et al 1980;Dahlof 1981;Patel et al 1981;Vanhoutte et al 1981;Majewski 1983;Osswald and GuimarHes 1983;Chesselet 1984;Gothert 1985;Misu and Kubo 1986;Borkowski 1988;Nedergaard and Abrahamsen 1990), the theory of feedback mechanisms has been questioned by a number of authors (Kalsner 1979a(Kalsner , b, 1980a(Kalsner , b, 1981(Kalsner , 1982a(Kalsner , b, c, d, 1983a(Kalsner , b, 1984(Kalsner , 1985aKalsner and Chan 1979;…”

Section: Umentioning

confidence: 99%

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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“…Since the discovery of prejunctional dopamine receptors, many investigators have reported on the neuroinhibitory activity of dopamine and dopamine analogues in a variety of in vivo and in vitro preparations (Clark, 1981; Costall & Naylor, 1981;Patel et al, 1981; Cavero, Massingham & Lefevre-Borg, 1982). The results obtained in several of these preparations have been used for classification of the dopamine receptor, and to provide a physiological correlate for receptor binding studies.…”

Section: Introductionmentioning

confidence: 99%

Neuronal Dopamine Receptors of the Rabbit Ear Artery: Pharmacological Characterization of the Receptor

Hieble¹,

Nelson

Steinsland

1985

Journal of Autonomic Pharmacology

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Dopamine and apomorphine were examined in the rabbit isolated perfused ear artery for both direct effects on vascular smooth muscle and effects on the response to field stimulation of sympathetic nerve terminals. The neuroinhibitory effect of both dopamine (EC50 = 37 nM) and apomorphine (EC50 = 44 nM) occurred at concentrations which did not produce vasoconstriction. The neuroinhibitory effect of dopamine was shown to be due to inhibition of noradrenaline release by measurement of 3H-overflow from prelabelled tissues. At relatively high concentrations dopamine produced vasoconstriction. In a superfused segment of ear artery, dopamine was found to be a full agonist at the alpha 1-adrenoreceptor, with an EC50 (15 microM) about 75 fold higher than the EC50 for noradrenaline. At concentrations up to 3 microM, apomorphine had no vasoconstrictor activity in the perfused ear artery. Representative examples of several classes of dopamine antagonists, including the phenothiazines, butyrophenones, diphenylbutylpiperidines and benzamides produced competitive antagonism of dopamine or apomorphine-induced inhibition, with nearly identical Kb values against these two agonists. The pharmacological characteristics of the neuronal dopamine receptor on the rabbit ear artery would indicate this receptor to be typical of the D2 subclass, and this tissue to be a useful model for quantitative studies on dopamine receptor agonists and antagonists.

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Regulation of catecholamine release by presynaptic receptor system

Cited by 29 publications

References 114 publications

Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

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

Neuronal Dopamine Receptors of the Rabbit Ear Artery: Pharmacological Characterization of the Receptor

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