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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 22 (1995), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effect of methoxamine, an α1-adrenoceptor agonist, on the overflow of endogenous noradrenaline (NA) was examined in the electrically field stimulated (EFS) caudal artery obtained from Wistar rats, Wistar-Kyoto rats (WKY) and age-matched spontaneously hypertensive rats (SHR).2. Methoxamine inhibited the EFS-evoked release of endogenous NA in the arteries from Wistar rats and WKY, but not in the arteries of SHR. 2-chloroadenosine, a purinoceptor agonist, also inhibited the NA release in the arteries from normotensive rats but not in the arteries of SHR.3. The inhibitory effect of methoxamine was blocked by adenosine deaminase and potentiated by adenosine uptake inhibitor, dipyridamole.4. Methoxamine caused the release of adenine nucleotides and adenosine from the caudal arteries of WKY and SHR.5. These suggest that the inhibitory effect of methoxamine on NA release is mediated by endogenous adenyl purines and that the failure of methoxamine to inhibit NA release in the caudal artery of SHR is due to a dysfunction of the pre-junctional purinoceptors on sympathetic nerve terminals.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effect of NG-nitro-l-arginine (NO2Arg) on the relaxation of canine basilar artery was investigated and compared with those of middle cerebral and femoral arteries.2. NO2Arg (10−7-3 × 10−5 mol/L) inhibited the substance-P (Sub-P; 10−12-10−8 mol/L) induced relaxation in the basilar artery precontracted with prostaglandin F2α (PGF2α; 10−5 mol/L) or KCl (10−2 mol/L) in a concentration-dependent manner and a ratio of the maximum inhibition by NO2Arg (3 × 10−5 mol/L) was more than 90%.3. The relaxation induced by A23187 (10−9-3 × 10−6) was also abolished by NO2Arg (3 × 10−5 mol/L), but that by glyceryl trinitrate (GTN; 10−9-3 × 10−5 mol/L) was not, in the basilar artery precontracted with PGF2α (10−5 mol/L). NG-nitro-d-arginine (NO2ArgD; 3 × 10−5 mol/L) did not affect the relaxation induced by Sub-P (10−12-10−8 mol/L).4. l-arginine (l-Arg; 3 × 10−5-10−4 mol/L) did not inhibit Sub-P (10−12-10−8 mol/L) induced relaxation in the basilar artery. Pretreatment of l-Arg (10−4 mol/L) reversed the relaxation inhibited by NO2Arg (3 × 10−6 mol/L) in the arteries.5. NO2Arg (3 × 10−5 mol/L) inhibited the Sub-P (10−12-10−8 mol/L) induced relaxation in the canine middle cerebral artery as much as in the basilar artery. NO2Arg (3 × 10−5 mol/L) also inhibited Sub-P (10−12-10−8 mol/L) induced relaxation in the femoral artery, but the degree of the inhibition was less than that in the basilar artery.6. These results suggest that the endothelium-derived relaxing factor (EDRF) of canine basilar artery is mainly l-Arg derived nitric oxide which may play a more important role in the basilar artery than the femoral artery.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. To determine the α-adrenergic receptor subtypes that affect the microcirculation of skin, the relative absorption (RA) spectra of the skin on the backs of rats were measured using reflectance spectrophotometric methods. We injected α-adrenergic agonists, noradrenaline (NA), phenylephrine (PE) and clonidine (CL), intravenously and determined changes in the RA value at 569 nm, one of the isosbestic points of the oxyhaemoglobin and deoxyhaemoglobin absorption.2. NA reduced the RA value and the reduction was inhibited significantly by pretreatment with phenoxybenzamine (PBZ; P〈0.01). These findings suggested that the haemoglobin content in the skin tissue decreased as a result of vasoconstriction through α-adrenoceptors.3. NA, PE and CL produced dose-dependent reductions in RA. CL and NA produced virtually equipotent reductions except at the highest dose used. PE produced smaller effects. The potency of these drugs in terms of changes in RA did not correlate with their potency in terms of rises in systemic blood pressure (NA ≤ PE ≥ CL).4. Yohimbine (YO) inhibited the NA-induced reduction in RA to a greater degree than bunazosin (BU). Midaglizole, a specific α2-adrenergic antagonist, significantly and dose dependently inhibited the NA-induced reduction in RA.5. Although BU inhibited NA-induced reduction in RA only slightly, the effect was significant (P〈0.05). BU significantly inhibited PE-induced reduction (P〈0.01), but did not inhibit CL-induced reduction.6. These observations suggest that the microcirculation of the skin of the rat is affected mainly by α2-adrenoceptor mediated vasoconstriction. However, α1-adrenoceptor mediated vasoconstriction also has some effect.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. NG-nitro-L-arginine (NO2Arg) is a guanidine nitro arginine derivative and an inhibitor of endothelium-dependent vascular relaxation. Significant rise of the systolic blood pressure was observed after 1 week administration of NO2Arg in food (0.023% in weight, about 2.8 mg of NO2Arg/rat per day) in female rats of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The rises were not different between SHRSP (21 mmHg) and WKY (23 mmHg).2. In ring preparations of the thoracic aorta of NO2Arg-administered rats of both strains, relaxation by acetylcholine decreased markedly compared with those of the control rats (to 43–44%). On the contrary, glyceryltrinitrate-induced relaxation was slightly but significantly increased in the aorta of WKY after NO2Arg administration and the same tendency was observed in SHRSP.3. The rise of blood pressure and the decrease of acetylcholine-induced relaxation suggested that NO2Arg inhibited the endothelium-dependent relaxation not only in WKY but also in SHRSP. The relaxation of the thoracic aorta preparation of SHRSP by acetylcholine was much less (ca 38%) than that of WKY; however, that of SHRSP by glyceryltrinitrate was slightly less (ca 74%), indicating that endothelium-dependent relaxation declined in vascular preparation of SHRSP.4. The present results suggest that endothelium-dependent relaxation has some contribution on blood pressure regulation in the hypertensive state, although a decline of endothelium-dependent relaxation is evident in vascular preparation of SHRSP compared with WKY.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 24 (1997), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effects of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthase inhibitor, on the microcirculation of rat dorsal skin were studied to examine the role of NO in the regulation of regional haemodynamics.2. The blood volume in the skin microcirculation, which was continuously measured by reflectance spectrophotometry, was significantly decreased in response to L-NMMA (10 mg/kg bodyweight, i.v.), suggesting vasoconstriction, and the response continued for more than 20 min. In contrast, the increase in systemic blood pressure (BP) disappeared soon after administration of L-NMMA.3. These results show that L-NMMA elicits long-lasting responses in the skin microcirculation, whereas the systemic BP rapidly recovers, suggesting a large contribution of the NO system to the regulation of rat skin microcirculation.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Change with time of the content and uptake of dopamine (DA) and noradrenaline (NA) in the renal, superior mesenteric and femoral arteries and abdominal aorta of rabbit after reserpine administration was examined. Endogenous DA and NA were measured by high performance liquid chromatography coupled with electrochemical detector.2. A single dose of reserpine (3 mg/kg, i.p.) maximally depleted the endogenous DA and NA contents in the four blood vessels 24 h after the administration; the ratios of reductions were 70–90% and approximately 90% of the normal levels, respectively. The DA contents in all four vessels recovered to the normal level within 4 days after reserpine. However, NA content did not recover to the normal levels within 30 days after reserpine except in the mesenteric artery.3. The activity of dopamine β-hydroxylase (DBH) significantly increased in all four blood vessels 1 h after reserpine. Although the DBH activity returned to the normal level after 3 days in the mesenteric artery, it returned within 24 h in the other three vessels.4. [3H]-Dopamine and [3H]-NA uptake were almost completely depressed 1 h after reserpine. The [3H]-NA uptake in four vessels recovered to the normal level 2–14 days after reserpine, and [3H]-DA uptake recovered after 30–45 days. Thus, the endogenous DA content in blood vessels was completely restored although DA uptake and NA content were still affected.5. These results suggested that the recovery of stored DA after reserpine was faster than that of stored NA and the recovery of DA uptake after reserpine was slower than NA uptake. This indicates a possibility that a part of DA pool may be different from NA pool in adrenergic nerve terminals in the blood vessels.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Effects of administration of NG-nitro-L-arginine (NO2Arg), a guanidino nitroarginine derivative, for 1 week on blood pressure and some vascular responses of rats were studied.2. A significant rise of the systolic blood pressure was observed after the administration of NO2Arg with food (0.023% in weight, about 2.8 mg of NO2Arg per rat per day). Relaxation by acetylcholine decreased markedly in ring preparations of the thoracic aorta of NO2Arg-treated rats. However, glyceryltrinitrate-induced relaxation was not reduced after NO2Arg administration, suggesting that NO2Arg administration specifically inhibited endothelium-dependent relaxation.3. An increase of blood pressure may be because oral administration of NO2Arg inhibited endothelium-dependent relaxation in vivo suggesting that the release of EDRF is important in physiological control of blood pressure.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 19 (1992), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The relaxing response of dopamine (DA) was studied in the rabbit pulmonary artery. DA caused concentration-related relaxation in helically cut strips of the artery contracted with prostaglandin F2α in the presence of prazosin.2. The DA-induced relaxation in endothelium-denuded strips was reduced to about 40% compared with that in endothelium-intact strips.3. Methylene blue and haemoglobin, inhibitors of endothelium-dependent relaxation, reduced the DA-induced relaxations in endothelium-intact strips to the level of endothelium-denuded strips. These results indicate that the DA-induced relaxation is partially mediated or modified by the release of endothelium-derived relaxing factor (EDRF).4. Apomorphine, as a DA agonist, caused concentration-dependent relaxation in endothelium-intact strips. Bromocriptine, a DA2 agonist, produced only a little relaxation at higher concentration.5. In endothelium-intact strips, haloperidol, a DA antagonist, and the DA1 antagonists, fluphenazine and SCH 23390 inhibited DA-induced relaxations. On the other hand spiperone and domperidone, DA2 antagonists, were inactive.6. In endothelium-denuded strips, fluphenazine and SCH 23390 inhibited DA-induced relaxations, but domperidone was inactive.7. These results indicate that the DA-induced relaxation is mediated by DA receptors, and that DA1 receptors are involved in both endothelium-dependent and-independent relaxation in the rabbit pulmonary artery.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1912
    Keywords: Methoxamine ; ATP ; Rabbit ear artery ; Transjunctional modulation ; Prejunctional purinoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of methoxamine, an α1-adrenoceptor agonist, on the electrically-evoked release of endogenous noradrenaline was examined in the isolated rabbit ear artery. Noradrenaline was quantified by high performance liquid chromatography-electrochemical detection. The release of adenine nucleotides and nucleosides by methoxamine was examined using high performance liquid chromatography-fluorescence detection. The release of noradrenaline evoked by electrical field stimulation (EFS) at 4 Hz was reduced by tetrodotoxin 0.3 μmol/l and clonidine 1 μmol/l by approximately 80% and 50%, respectively. On the other hand, methoxamine at 10 but not 1 μmol/l enhanced the release of noradrenaline to approximately twice the control, and the enhancement was prevented by prazosin 1 μmol/l. The facilitatory action of methoxamine was also abolished after desensitization of P2-purinoceptors by α,β-methylene ATP 30 μmol/l as well as by the presumed P2-purinoceptor antagonist suramin given at 10 μmol/l. Exogenous ATP 10 μmol/l significantly enhanced the EFS-evoked release of noradrenaline, and the enhancement was abolished by α,β-methylene ATP and suramin. None of the drugs changed the spontaneous outflow of noradrenaline. These results indicate that endogenous ATP, acting at prejunctional purinoceptors, may participate in the facilitatory effect of methoxamine. Indeed, methoxamine 10 μmol/l significantly enhanced the spontaneous outflow of ATP and, less so, ADP. The methoxamine evoked release of ATP and ADP was antagonized by prazosin 1 μmol/l. It is concluded that methoxamine releases endogenous ATP from postjunctional sites which then, via prejunctional purinoceptors, facilitates action potential-evoked release of noradrenaline in rabbit ear artery.
    Type of Medium: Electronic Resource
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