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ABSTRACT: 1. The vasoconstrictor response to periarterial nerve electrical stimulation (PNS) and neurotransmission by ATP are discussed and illustrated, using canine isolated and perfused splenic arterial preparations. 2. The conditions for appearance of dominant purinergic constrictor response to PNS are discussed. 3. Modulation of the purinergic vasoconstrictor responses to PNS by several kinds of presynaptic receptor agonists and antagonists is reviewed. 4. Influences of purinergic responses to PNS by guanethidine, reserpine, tetrodotoxin (TTX) or omega-conotoxin GVIA (omegaCTX) are also reviewed. 5. Effects of imipramine and removal of the endothelium are discussed. 6. Evidence is presented for selective inhibition of purinergic responses to PNS by an adequate cold storage of the vessel. 7. The roles of ATP released by PNS in isolated canine splenic arteries are proposed.
Autonomic & Autacoid Pharmacology 05/2003; 23(2):95-104.
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ABSTRACT: Summary1 The present study attempted to pharmacologically characterize the subtypes of α-adrenoceptors mediating the vasoconstriction in the isolated and perfused canine vesical artery.2 Noradrenaline (NA) and phenylephrine (PE, an α1-adrenoceptor agonist) induced a dose-dependent vasoconstriction, whereas xylazine (an α2-agonist) did not induce any clear vascular constrictor response.3 Prazosin at 0.01 μm and rauwolscine at 0.1 μm failed to affect the NA-induced vasoconstriction. Prazosin at 0.1 μm antagonized the vasoconstrictor responses to NA, with pKB value of 7.8.4 WB 4101 at 0.01–0.1 μm dose-dependently inhibited the responses to NA, with a pKB value of 8.9. The vasoconstrictor responses to NA were not significantly affected by chloroethylclonidine (10–30 μm) or BMY 7378 (0.1 μm).5 The present results indicate that the canine vesical arteries dominantly contain α1-adrenoceptors but have no α2-adrenoceptors, and the functional subtype of α1-adrenoceptor is characterized as an α1A-adrenoceptor subtype.
Autonomic & Autacoid Pharmacology 04/2003; 22(5‐6):253 - 259.
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ABSTRACT: 1 The effects of neuropeptide Y (NPY) upon the isolated vasculature are reviewed. 2 The vasconstrictor responses to periarterial nerve stimulation (PNS) and neurotransmission by noradrenaline (NA) and ATP are discussed and illustrated using canine isolated perfused splenic artery. 3 Modulation of the vascular responses to PNS by NPY via pre- and post-junctional NPY Y2 and Y1 receptors is discussed. 4 Evidence is presented for different alpha1-adrenoceptor subtypes mediating vasoconstriction to exogenous and endogenously released NA and their different locations in the neurovascular junction and extrajunctional regions. 5 Activation of NPY Y1-receptors potentiates sympathetic nerve activated alpha1-adrenoceptor vasoconstriction. The proposal that the postjunctional alpha1B adrenoceptor may be linked to the NPY Y1-receptor and is responsible for co-operation between sympathetic and NPYergic interactions in the vasculature is discussed.
Autonomic & Autacoid Pharmacology 09/2002; 22(4):187-97.
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ABSTRACT: We studied the binding properties of KRH-594, a new selective antagonist of angiotensin II (AII) type 1 (AT1) receptors, to rat liver membranes and to recombinant AT1 and AT2 receptors. Preincubation of rat liver membranes with KRH-594 produced maximal inhibition of [125I]-AII binding when the preincubation time was 1-2 h. Preincubation with KRH-594 for 2 h decreased the B(max) value and increased the Kd value. For human AT1, human AT2, rat AT1A and rat AT1B receptors, the Ki values for KRH-594 were 1.24, 9360, 0.67, and 1.02 nm, respectively. The rank order of K1 values for human AT1 receptors was KRH-594 > EXP3174 > candesartan = AII. The order of specificities for human AT1 and AT2 receptors was candesartan > EXP3174 > KRH-594. Although a 2-h preincubation of human AT2 receptors with KRH-594 (30 microM) or CGP 42112 (a selective AT2 receptor antagonist; 0.3 nM) inhibited binding of [125I]-AII, the suppression by KRH-594 was not significant. These results indicate that KRH-594 binds potently to AT1 receptors in an insurmountable manner, and that at a very high dose (30 microM) it may also bind to AT2 receptors, but in a surmountable manner.
Fundamental and Clinical Pharmacology 08/2002; 16(4):317-23. · 1.80 Impact Factor
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ABSTRACT: 1 The effects of BIIE 0246, a novel and non-peptide neuropeptide Y (NPY) Y2 receptor antagonist on sympathetic vasoconstriction of the canine splenic artery were investigated. 2 The vasoconstrictor response to periarterial electrical nerve stimulation was described to be a double peaked vasoconstriction consisting of an initial transient, dominantly P2X purinoceptor-mediated constriction followed by a prolonged, mainly alpha1 adrenoceptor-induced response. 3 BIIE 0246 at a concentration of 0.1-1 microM dose-dependently potentiated double peaked constrictions at low frequencies (1 and 4 Hz), whereas at high frequency (10 Hz), it failed to affect these responses. BIIE 0246 (1 microM) also enhanced double peaked responses even in the presence of rauwolscine (0.1 microM). NPY (13-36) (1-100 nM), a selective Y2 receptor agonist reduced these two peaked responses in a dose-related manner. The vasoconstriction to noradrenaline (0.1-10 nmol) or adenosine triphosphate (0.01-1 micromol) was not significantly influenced by either 1 microM BIIE 0246 or 100 nM NPY (13-36). Exposure of tissues to 1 microM BIIE 0246 almost completely prevented the suppression of double peaked constrictions by NPY (13-36) (10 nM) or by NPY (10 nM). 4 We conclude that NPY inhibits sympathetic purinergic and adrenergic vasoconstrictions through an activation of prejunctional Y2 receptor subtype in the neurovascular junction of the canine splenic artery.
Autonomic & Autacoid Pharmacology 05/2002; 22(2):119-26.
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ABSTRACT: Our previous study demonstrated that the vasoconstrictor responses to trains of up to 10 pulses at 1 Hz of stimulation appeared to be purinergic monophasic, whereas a longer train of 30 pulses induced a biphasic vasoconstriction consisting of an initial, transient purinergic constriction followed by a prolonged adrenergic response. Neuropeptide Y (NPY) at doses of 0.01 and 0.1 microM produced a dose-dependent inhibition on the monophasic and biphasic vasoconstrictor responses to nerve stimulation. The treatment with Leu31 Pro34 neuropeptide Y (LP-NPY) (0.03 microM) did not affect the monophasic responses to short pulse trains of stimulation. However, LP-NPY markedly potentiated the second phase response to 30 pulse trains of stimulation, although it did not modify the first one. The LP-NPY-induced potentiation was abolished by BIBP 3226 (1 microM), a selective NPY Y1 receptor antagonist. The results indicate that the activation of NPY Y1 receptors may enhance the prolonged adrenergic vasoconstriction but not the transient purinergic response in the canine splenic artery.
Journal of Cardiovascular Pharmacology 11/2001; 38 Suppl 1:S17-20. · 2.29 Impact Factor
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ABSTRACT: 1. The present study attempted to pharmacologically characterize the alpha-adrenoceptor subtypes mediating vasoconstriction in canine isolated and perfused mandibular alveolar artery (MAA). 2. Noradrenaline (NA) and phenylephrine (PE) induced a strong vasoconstriction in a dose-dependent manner. The PE-induced vascular constriction was significantly inhibited by treatment with prazosin. Xylazine evoked a moderate vascular constriction and the xylazine-induced response was suppressed by rauwolscine. The NA-induced response was partially inhibited by rauwolscine and the remaining response to NA was abolished by subsequent administration of prazosin. 3. Treatment of MAA with WB4101 produced a dose-dependent inhibition of NA-induced vasoconstriction. Pretreatment of tissues with 10 micromol/L chloroethylclonidine produced a slight and statistically significant inhibition of NA-induced responses. BMY 7378, a selective alpha(1D)-adrenoceptor antagonist, failed to significantly affect vasoconstrictor responses to NA. 4. The present results suggests that: (i) both alpha(1)- and alpha(2)-adrenoceptors are involved in vasoconstrictor responses in the canine MAA; and (ii) the alpha(1)-adrenoceptors involved in the vasoconstrictor responses in the MAA are characterized as mainly of the alpha(1A)- and partially of the alpha(1B)-adrenoceptor subtype.
Clinical and Experimental Pharmacology and Physiology 10/2001; 28(9):716-20. · 1.85 Impact Factor
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ABSTRACT: The isolated canine atrium was perfused by heparinized blood of the donor dog. An adequate dose of pentobarbital that induced a potent hypotension in the donor did not produce any significant change in the atrial rate and developed tension in the isolated atrium perfused with donor's blood. Pentobarbital in doses that modified neither cardiac responses to intracardiac adrenergic nerve stimulation nor exogenously given norepinephrine or acetylcholine significantly inhibited intracardiac vagal responses. From these results, it is concluded that a large dose of pentobarbital has a dominant antivagal effect in the heart.
The Japanese Journal of Pharmacology 07/2001; 86(2):248-50.
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ABSTRACT: The present study attempted to characterize the alpha(1)-adrenoceptor subtypes mediating vasoconstrictor responses to administered and nerve stimulation-evoked noradrenaline (NA) release in the isolated and perfused canine splenic artery. A previous study demonstrated that periarterial electrical nerve stimulation (30 s trains of pulses at a frequency of 1, 4 or 10 Hz) induced a double peaked vasoconstriction consisting of an initial transient, predominantly P2X-purinoceptor-mediated constriction followed by a prolonged, mainly alpha(1)-adrenoceptor-mediated response in the canine splenic artery. The effects of alpha(1)-adrenoceptor subtype antagonists on neuronally-mediated second peaked vasoconstrictions were analysed. BMY 7378 (10 - 100 nM), a selective alpha(1D)-adrenoceptor antagonist produced a dose-dependent inhibition of the second peak responses at all frequencies used. BMY 7378 (100 nM) reduced these responses by approximately 30%. Exposure of tissues to chloroethylclonidine (CEC, 60 microM), a selective alpha(1B)-adrenoceptor antagonist attenuated the second peak response by approximately 60%, even in the presence of BMY 7378 (100 nM). On the other hand, WB 4101 (100 nM), a selective alpha(1A)-adrenoceptor antagonist potentiated nerve-stimulation-evoked double peaked vasoconstrictions, especially at low frequencies (1 and 4 Hz). Vasoconstrictor responses to administered NA were dose-dependently antagonized by WB 4101 (10 - 100 nM), but were not significantly affected by either BMY 7378 (10 - 100 nM) or by CEC (60 microM). The present results indicate that NA released from sympathetic nerves may junctionally exert its vasoconstrictor effect via activation of postjunctional alpha(1B)- and in part alpha(1D)-adrenoceptors, whereas exogenous NA extrajunctionally activates alpha(1A)-adrenoceptors to produce its vascular action in canine splenic arteries.
British Journal of Pharmacology 05/2001; 132(8):1852-8. · 4.41 Impact Factor
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ABSTRACT: 1. Using the cannula inserting method, vasodilator responses to beta-adrenoceptor agonists (isoprenaline, denopamine and procaterol) were investigated in isolated and perfused rat common carotid arteries. 2. Each beta-adrenoceptor agonist induced a vasodilation in preparations preconstricted by phenylephrine in a dose-related manner. The potencies were in the order of isoprenaline > procaterol > denopamine. 3. Denopamine-induced dilations were significantly inhibited by 1 nmol betaxolol (a selective beta1-adrenoceptor antagonist), but it was not influenced by 1 nmol ICI 118,551 (a selective beta2-adrenoceptor antagonist). On the other hand, procaterol-induced vasodilations were significantly inhibited by 1 nmol ICI 118,551 but not modified by 10 nmol betaxolol. 4. ACh-induced vasodilations disappeared after intraluminal saponin injection to remove endothelium, but procaterol- and denopamine-induced dilations were not modified by removal of the endothelium. 5. Pretreatment with L-NG-nitroarginine methyl ester (L-NAME) readily inhibited ACh-induced vasodilations. However, neither procaterol- or denopamine-induced vasodilation was modified by L-NAME treatment. 6. From these results, it is concluded that in the rat common carotid arteries (1) there are abundant beta2- and a few beta1-adrenoceptors, and (2) there is no participation of the endothelium-dependent mechanism in beta-adrenoceptor mediated vasodilations.
Journal of Autonomic Pharmacology 03/2001; 21(1):7-13.
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ABSTRACT: The periarterial electrical nerve stimulation at a frequency of 4 Hz (30-s trains of pulses) induced a double-peaked vasoconstriction in the canine splenic artery. The treatment with chloroethylclonidine (CEC, 60 microM) markedly inhibited the second-peaked constriction, whereas it produced an insignificant effect on the first-peaked response. The vasoconstriction to noradrenaline (NA, 1 nmol) was not significantly influenced by 60 microM CEC. On the other hand, WB 4101 (1 microM) consistently abolished the vascular response induced by NA (1 nmol), but rather potentiated the double-peaked constriction. The results indicate that neuronal NA may junctionally exert its vasoconstrictor effect via an activation of postjunctional alpha1B-receptors, whereas exogenous NA may extrajunctionally activate alpha1A-receptors for its vascular action in the canine splenic artery.
The Japanese Journal of Pharmacology 12/2000; 84(3):360-2.
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ABSTRACT: 1. The effects of temperature on submaximal vasoconstriction to an intraluminal administration of noradrenaline (NA), phenylephrine, tyramine and KCl were investigated in canine isolated and perfused lingual and mesenteric arteries, using the cannula-inserting method. 2. In lingual arteries, cooling (from 37 to 27 degrees C) caused significant depression of vasoconstriction to the four vasoactive substances used. Rewarming (to 37 degrees C) induced a significant augmentation of constriction by NA, phenylephrine and KCl, but not tyramine. 3. In mesenteric arteries, cooling depressed tyramine- and KCl-induced constrictions, but had no effect on NA- and phenylephrine-induced vasoconstriction. Only in the case of KCl-induced constrictions did rewarming induce a potentiation of the vasoconstrictor response. 4. We conclude that: (i) cooling induces a depression of voltage-dependent Ca2+ channels and rewarming may induce a potentiation of Ca2+ channels in both arteries; (ii) alpha1-adrenoceptor-operated Ca2+ channels are depressed by cooling in lingual arteries but not in mesenteric arteries; and (iii) cooling may induce an attenuation of the re-uptake function in sympathetic nerve terminals in both arteries and this attenuation may be not rapidly restored by acute rewarming.
Clinical and Experimental Pharmacology and Physiology 12/2000; 27(11):876-80. · 1.85 Impact Factor
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ABSTRACT: The rat homologue of the human M(r) 110000 antigen, which cross-reacts with anti-carcinoembryonic antigen antibodies, was isolated from a rat lung cDNA library. The deduced amino acid sequence revealed a signal peptide, cysteine-rich and immunoglobulin-like region, serine-threonine region, and N-glycosylation sites in the extracellular portion. Northern blot analysis demonstrated a wide distribution of the mRNA in adult rat tissues and A10 rat vascular smooth muscle cells. Therefore, the rat homologue of the human M(r) 110000 antigen may be a receptor or a cell adhesion molecule rather than a specific carcinogenic antigen.
Biochimica et Biophysica Acta 11/2000; 1493(3):378-82. · 4.66 Impact Factor
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ABSTRACT: Some parasympathetic ganglionic cells are located in the epicardial fat pad between the medial superior vena cava and the aortic root (SVC-Ao fat pad) of the dog. We investigated whether the ganglionic cells in the SVC-Ao fat pad control the right atrial contractile force, sinus cycle length (SCL), and atrioventricular (AV) conduction in the autonomically decentralized heart of the anesthetized dog. Stimulation of both sides of the cervical vagal complexes (CVS) decreased right atrial contractile force, increased SCL, and prolonged AV interval. Stimulation of the rate-related parasympathetic nerves to the sinoatrial (SA) node (SAPS) increased SCL and decreased atrial contractile force. Stimulation of the AV conduction-related parasympathetic nerves to the AV node prolonged AV interval. Trimethaphan, a ganglionic nicotinic receptor blocker, injected into the SVC-Ao fat pad attenuated the negative inotropic, chronotropic, and dromotropic responses to CVS by 33 approximately 37%. On the other hand, lidocaine, a sodium channel blocker, injected into the SVC-Ao fat pad almost totally inhibited the inotropic and chronotropic responses to CVS and partly inhibited the dromotropic one. Lidocaine or trimethaphan injected into the SAPS locus abolished the inotropic responses to SAPS, but it partly attenuated those to CVS, although these treatments abolished the chronotropic responses to SAPS or CVS. These results suggest that parasympathetic ganglionic cells in the SVC-Ao fat pad, differing from those in SA and AV fat pads, nonselectively control the atrial contractile force, SCL, and AV conduction partially in the dog heart.
AJP Heart and Circulatory Physiology 10/2000; 279(3):H1201-7. · 3.71 Impact Factor
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ABSTRACT: We investigated the effects of a continuous infusion of adenosine on responses of sinus rate and developed tension to bolus injections of adenosine and acetylcholine in isolated, blood-perfused canine right atria. Each drug was directly injected into the sinus node artery of the isolated atrium. During adenosine infusions, the negative chronotropic and inotropic responses to bolus injections of adenosine were significantly inhibited in a dose-related manner, while the negative responses to administered acetylcholine were consistently potentiated. These results indicate that adenosine infusion has an acute desensitizing action on subsequent bolus adenosine, although the cholinergic action is enhanced by a continuous infusion of adenosine.
The Japanese Journal of Pharmacology 09/2000; 83(4):348-50.
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ABSTRACT: The periarterial electrical nerve stimulation (30 s trains of pulses at a frequency of 1, 4 or 10 Hz) induced a double peaked vasoconstriction consisting of an initial transient constriction (first peak) followed by a prolonged response (second peak) in the isolated, perfused canine splenic artery. At low frequencies (1 and 4 Hz), a neuropeptide Y (NPY) Y(1) receptor antagonist BIBP 3226 (0.1-1 microM) produced a dose-dependent inhibitory effect on the second peak, but did not modify the first peak. At a high frequency (10 Hz), 1 microM BIBP 3226 induced a slight, but significant inhibition on both the first and second peaked responses. At a low frequency (1 Hz), the first peak was not influenced by blockade of alpha(1)-adrenoceptors or NPY Y(1) receptors with prazosin (0.1 microM) or BIBP 3226 (1 microM), respectively, but abolished by P2X receptor desensitization with alpha,beta-methylene ATP (alphabeta-m ATP, 1 microM). At a high frequency (10 Hz), the first peak was mostly inhibited by alphabeta-m ATP and partially by prazosin and BIBP 3226. On the other hand, the second peak at a low frequency was largely decreased by BIBP 3226 and partially by prazosin and alphabeta-m ATP, whereas at a high frequency, it was largely attenuated by prazosin and partially by alphabeta-m ATP and BIBP 3226. The results suggest that at a low frequency, the firstly transient constriction of double peaked responses is mainly induced via an activation of P2X-receptors, whereas at a high frequency, it is mostly mediated by the P2X-receptors, and partially by alpha(1)-receptors and NPY Y(1)-receptors. The secondary prolonged vasoconstriction at frequencies used is predominantly mediated via both alpha(1)-receptor and NPY Y(1) receptor activations, and in part by P2X-receptors. Furthermore, an activation of NPY Y(1) receptors may play an important role in evoking the prolonged vasoconstrictor response to longer pulse trains of stimulation at a low frequency, whereas an alpha(1)-adrenoceptor activation exerts a main vasomotor effect for the prolonged response at a high frequency.
British Journal of Pharmacology 09/2000; 130(7):1699-705. · 4.41 Impact Factor
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ABSTRACT: The effect of temperature on submaximal vasoconstrictions to an intraluminal injection of serotonin (5-HT) and methoxamine was investigated in isolated and perfused canine lingual and mesenteric arteries, using the cannula insertion method. In both arteries cooling (from 37 degrees C to 27 degrees C) caused a remarkable enhancement of vasoconstriction to 5-HT, but did not to methoxamine. In lingual arteries, methoxamine-induced constrictions were strongly depressed, although those were slightly depressed in mesenteric arteries. It is assumed that 5-HT produces an important role to modulate vascular tonicity in low temperature conditions.
The Tohoku Journal of Experimental Medicine 08/2000; 191(3):139-44. · 1.24 Impact Factor
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ABSTRACT: The present study observed the effects of an activation of neuropeptide Y (NPY) Y1 receptors on adrenergic and purinergic components of double-peaked vasoconstrictor responses to periarterial nerve stimulation in the isolated, perfused canine splenic arteries. The results showed that 3-30 nM Leu31 Pro34 neuropeptide Y (LP-NPY) produced a dose-dependent potentiation of double-peaked vasoconstrictor responses to trains of 30-s pulses at 1, 4 or 10 Hz of stimulation. The potentiation of LP-NPY of the nerve-stimulated vasoconstrictions were completely inhibited by subsequent blockade of alpha1-adrenoceptors or Y1 receptors with 0.1 microM prazosin or with 1 microM BIBP 3226 ((R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-argininami de), respectively. The remaining responses in the presence of LP-NPY and prazosin were abolished by P2X receptor desensitization with 1 microM alpha,beta-methylene ATP. Moreover, 30 nM LP-NPY failed to modify the vasoconstrictor responses to nerve stimulation after treatment with prazosin. A subsequent administration of alpha,beta-methylene ATP completely suppressed the remaining responses after prazosin and LP-NPY. The vasoconstrictions induced by 0.003-1 nmol noradrenaline and 0.003-1 micromol ATP were slightly, but not significantly enhanced by 30 nM LP-NPY. The observations indicated that activation of postjunctional NPY Y1 receptors may have an important role in the modulation of adrenergic rather than purinergic transmission of the sympathetic co-transmission.
The Japanese Journal of Pharmacology 08/2000; 83(3):197-205.
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ABSTRACT: 1. Cardiac effects of lignocaine on sinoatrial nodal pacemaker activity and atrial contractility were investigated in five canine isolated, blood-perfused right atria that were perfused with heparinized blood from support dogs. The effects of lignocaine on responses to intracardiac nerve stimulation and administered acetylcholine and noradrenaline were also examined. 2. Lignocaine was injected into the support dog intravenously or administered selectively to the sinus node artery of the isolated atrium. At doses that did not produce significant depressor action (0.3, 1.0 and 3.0 mg/kg), lignocaine produced no significant changes in heart rate. A large dose of 10 mg/kg lignocaine caused significant depressor effects and slight bradycardia. Direct administration of lignocaine (0.3, 1.0, 3.0, 10.0 and 30.0 mumol) into the sinus node artery of the isolated atrium consistently caused slight negative chronotropic and rather marked negative inotropic effects. 3. After treatment with a relatively large dose of lignocaine, electrical stimulation-induced negative chronotropic and inotropic responses were significantly inhibited in a dose-related manner, but positive chronotropic and inotropic responses were slightly depressed only at an extremely high dose of lignocaine (10.0 mumol). 4. Noradrenaline-induced positive chronotropic and inotropic effects were not modified by any doses of lignocaine used (0.3, 1.0, 3.0 and 10.0 mumol). Acetylcholine-induced negative chronotropic and inotropic effects were slightly, but significantly, depressed by 10 mumol lignocaine. 5. These results suggest that a relatively large dose of lignocaine has a dominant presynaptic inhibitory action, particularly on the parasympathetic component.
Clinical and Experimental Pharmacology and Physiology 08/2000; 27(7):508-12. · 1.85 Impact Factor
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ABSTRACT: Complementary DNA of mouse deafness dystonia peptide 1 (DDP1) was isolated from adipocyte cDNA library and expressed in mammalian cells. The sequence shares homology of 92 and 97% on the nucleic acid and the amino acid levels with human DDP1. In comparison to mouse Bruton's tyrosine kinase (Btk) locus, the coding region spans 2 exons and the splice point is the same as human DDP1. Northern blot analysis suggests that mouse DDP1 expresses ubiquitously. In vitro transcription/translation study showed that the cDNA of mouse DDP1 codes about 11 kDa peptide. DDP1 tagged with FLAG localized in mitochondria and cytoplasm of COS7 cells. P19 embryonal carcinoma cells transfected with anti sense DDP1 cDNA were frequently dead after subculture and all the survivals expressed endogenous DDP1 mRNA. Therefore, mouse DDP1 may play an important role to survive in contrast to Tim8p, a yeast homologue, which was unnecessary in yeast.
Biochemical and Biophysical Research Communications 08/2000; 273(2):759-64. · 2.48 Impact Factor
