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  • 1
    Electronic Resource
    Electronic Resource
    The effects of hypochlorite-induced oxidative stress on presynaptic M2-receptors at sympathetic nerve endings in the rat tail artery (2002)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 22 (2002), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary 1 It was shown recently that stimulation of cardiac muscarinic M2-receptors revealed an enhanced negative inotropic response in isolated rat left atria after exposure to hypochlorite-induced oxidative stress. This phenomenon was not observed after stimulation of the cardiac A1-receptor, which like the M2-receptor is coupled to Gi-proteins. Since even the contractile response to M3-receptor stimulation was not amplified in the rat portal vein, we hypothesized a M2-receptor specificity of this hypochlorite-induced enhancement. 2 The present study was performed in order to investigate whether the sympathoinhibitory response to presynaptically located M2-receptor stimulation would also be modified after exposure to hypochlorite in the rat tail artery. We applied electrical field stimulation (EFS) in order to mimic sympathetic neurotransmission. 3 EFS increased the vascular tone frequency-dependently (0.3–4 Hz). EFS-induced vasoconstriction could be attenuated by acetylcholine (30 nm−1 μm) in a concentration-dependent manner. Hypochlorite (10 and 100 μm) did not affect the sympathoinhibitory effect of acetylcholine (100 nm). 4 In conclusion, in contrast to cardiac M2-receptors, hypochlorite did not amplify the sympathoinhibitory effects of presynaptic M2-receptors. The different responsiveness between neuronal and cardiac M2-receptors to hypochlorite may be explained by the different G-protein subunits involved in the activation of the underlying signalling cascade.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2002.00253.x
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  • 2
    Electronic Resource
    Electronic Resource
    Vasopressin-induced facilitation of adrenergic responses in the rat mesenteric artery is V1-receptor dependent (2003)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 23 (2003), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Notes: 1 The present study was designed to analyse the possible involvement of V1- and V2-receptors in vasopressin (AVP)-induced facilitation of the sympathetic nervous system. Furthermore, we aimed to determine whether the site of facilitation by AVP is located pre- or postsynaptically. 2 Electrical field stimulation (EFS) was applied on the rat mesteric artery to activate the sympathetic nervous system. In addition, we evaluated the direct vascular effects of AVP. The postsynaptic effect of AVP on the sympathetic nervous system was investigated by exposing the vessels to exogenous noradrenaline. These experiments were performed in the absence or presence of selective V1 and V2 receptor antagonists SR 49059 and SR 121463, respectively. Desmopressin was applied as a selective V2 agonist. 3 The direct vasoconstrictor effect of AVP was antagonized by SR 49059 and not by SR 121463. Desmopressin neither showed any direct vasoconstrictor effect nor produced vasodilatation after a precontraction induced by noradrenaline (10 μm). The EFS-induced rise in vascular tone could be increased by a sub-pressor concentration of AVP. This fascilitation could be antagonized by SR 49059, but not by SR 121463. Desmopressin did not influence the increase in vascular tone during EFS. Vasoconstriction induced by exogenous noradrenaline could be facilitated by a sub-pressor concentration of AVP and this selective postsynaptic effect could be antagonized by V1-receptor blockade. 4 In conclusion, the AVP-induced facilitation of the sympathetic nervous system is completely V1-receptor dependent and at least partly postsynaptically mediated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1474-8673.2003.00274.x
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of Aging and Hypertension on the Reactivity of Isolated Conduit and Resistance Vessels
    Amsterdam : Elsevier
    Microvascular Research 48 (1994), S. 303-315 
    Details
    ISSN: 0026-2862
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1006/mvre.1994.1057
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  • 4
    Electronic Resource
    Electronic Resource
    Thyroid hormone modulates inotropic responses, α-adrenoceptor density and catecholamine concentrations in the rat heart (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 755-764 
    Details
    ISSN: 1432-1912
    Keywords: Calcium handling ; α1-adrenoceptors ; Hyperthyroidism ; Hypothyroidism ; Tissue catecholamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the influence of hyper- and hypothyroidism on basal parameters of isolated perfused hearts of rats. In addition the effects of different extracellular calcium concentrations ([Ca2+]o), the calcium entry promoter Bay K8644 and the α1-adrenoceptor agonist methoxamine were investigated. Since alterations in α-adrenoceptor density could explain the increased sensitivity to methoxamine in hearts from hypothyroid rats, α1-adrenoceptor density in the left ventricle was also established. Different time-schedules of exposure to hyper- and hypothyroidism were used to investigate whether the influence of chronic dysthyroid states on α1-adrenoceptor density is transient and time-dependent. Simultaneously myocardial noradrenaline and adrenaline tissue concentrations were determined, since they might correlate with the observed changes. Hyperthyroidism was induced by feeding rats for 1, 4 and 8 weeks with 5 mg/kg L-thyroxine (T4)-containing rat chow. Hypothyroid rats were obtained by adding 0.05% propylthiouracil (PTU) to the drinking water during 1, 4 and 8 weeks. For the functional experiments animals were treated during 4 weeks, to mimic the clinical situation of a chronic endocrine disease. Langendorff hearts from hyperthyroid hearts showed an increased maximally developed relaxation velocity, whereas Langendorff hearts from hypothyroid rats showed an increased left ventricular pressure (LVP). We observed an increased maximal inotropic response to [Ca2+]o in hearts from both hyperthyroid and hypothyroid rats, indicating that both dysthyroid states interfere with the handling of calcium ions by the contractile apparatus. Unchanged responses to Bay K8644 in hearts from hyperthyroid and depressed responses in hearts from hypothyroid rats suggest that the involvement of L-type calcium channels is rather unlikely. Furthermore, the reflex increase in coronary flow in response to enhanced contractile force appeared to fail in hearts from hypothyroid rats. Sensitivity of the response to methoxamine was increased in hearts from hypothyroid rats, which was accompanied by a decrease in the number of myocardial α1-adrenoceptors. Both T4 and PTU treatment resulted in a non-transient decrease of α1-adrenoceptor density in left ventricular tissue. Furthermore, hypothyroidism increased the percentage of α1A-binding sites, whereas in hyperthyroidism the distribution of the α1-adrenoceptor subtypes was not affected. Myocardial tissue concencentrations of noradrenaline and adrenaline were unchanged in hyperthyroid rats and decreased in hypothyroid rats. The present study indicates that thyroid hormones have a direct rather than a sympathetically mediated effect on α1-adrenoceptor mediated myocardial functions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166902
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  • 5
    Electronic Resource
    Electronic Resource
    Characterization of the angiotensin II-receptor subtype in the longitudinal smooth muscle of the rat portal vein (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 220-224 
    Details
    ISSN: 1432-1912
    Keywords: Angiotensin II-receptor ; Dithiothreitol ; Nonpeptide angiotensin II-receptor antagonists ; Rat portal vein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The purpose of the present study was to identify the angiotensin II-receptor subtype involved in the enhancement of the amplitude of the phasic contractions by angiotensin II in the isolated rat portal vein preparation. At an extracellular Ca2+ concentration of 0.9 mmol/l and a K+ concentration of 4 mmol/l, angiotensin II induced concentration-dependent increases in the amplitude of the phasic contractions. The enhancement of phasic contraction amplitude caused by angiotensin II was not significantly altered by pretreatment of the rat portal vein with indomethacin 10−5 mol/l or nitro-L-arginine 10−4 mol/l, indicating that neither prostaglandins nor the endothelium derived-relaxing factor (NO) are involved. Losartan (DuP 753), a nonpeptide selective AT1-receptor antagonist, concentration-dependently shifted the concentration-response curve for the effect of angiotensin II on the amplitude of the contractions to the right, without reducing the maximal response (pA2 = 8.6, slope = 0.98), thus suggesting competitive antagonism at the level of AT1-receptors. By contrast, PD 123177, a nonpeptide selective AT2-receptor antagonist, even at 10−5 mol/l, caused no significant change of the phasic myogenic response to angiotensin II, indicating the absence of AT2-receptor involvement. Dithiothreitol, a disulfide-reducing agent which is known to inactivate AT1-receptors in various tissues, markedly inhibited (3 mmol/l) or even abolished (5 mmol/l) the contractile response of the rat portal vein to angiotensin II, supporting the conclusion that these receptors can be classified as AT1-receptors. In conclusion, the receptor subtype mediating the angiotensin II-induced potentiation of the spontaneous phasic contractions in the rat portal vein appears to belong to the AT1-receptor subtype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169271
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  • 6
    Electronic Resource
    Electronic Resource
    Positive inotropic action of angiotensin II in the pithed rat (1993)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 347 (1993), S. 658-663 
    Details
    ISSN: 1432-1912
    Keywords: Angiotensin II ; Myocardial contraction ; Pithed rat ; AT1 receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The cardiovascular effects of angiotensin II were examined in aortic blood pressure-controlled and-uncontrolled pithed rats. Angiotensin II induced a dose-dependent increase in diastolic blood pressure, left ventricular pressure (LVP), dP/dt (the first derivative of LVP) and heart rate in pithed rats. The maximal responses for these parameters were similar to those to noradrenaline, except for the rise in diastolic blood pressure, where noradrenaline caused a greater increase than angiotensin II. After treatment with propranolol, the positive chronotropic effect of angiotensin II was abolished. Angiotensin II produced a dose-dependent increase in diastolic blood pressure, which was similar to that of vasopressin, and an increase in dP/dtmax, which proved much greater than that of vasopressin. When aortic blood pressure was controlled and the β-receptors were blocked by propranolol, angiotensin II caused a dose-dependent increase in dP/dtmax without affecting the left ventricular enddiastolic pressure. The same results were obtained after both β- and α-adrenoceptors were blocked by propranolol and phentolamine. Losartan but not PD 123177 caused parallel rightward shifts of the dose-response curve of angiotensin II for dP/dtmax in the aortic blood pressure controlled pithed rat without altering the maximal response. It is concluded that in the pithed rat angiotensin II produced an increase in myocardial contractile force which is not mediated by β- or α-adrenoceptors. The inotropic effect appears to be mediated by angiotensin receptors, of the AT1-subtype.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166950
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  • 7
    Electronic Resource
    Electronic Resource
    The influence of hyperthyroidism on β-adrenoceptor-mediated relaxation of isolated small mesenteric arteries (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 438-444 
    Details
    ISSN: 1432-1912
    Keywords: Mesenteric resistance arteries ; Hyperthyroidism ; β-adrenoceptor agonists ; β2-adrenoceptor ; Second messenger system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We investigated the influence of hyperthyroidism on relaxant responses of small mesenteric resistance arteries to β-adrenoceptor agonists and to compounds stimulating the corresponding second-messenger system. Hyperthyroidism was induced by feeding rats for 28 days with 5 mg/kg L-thyroxine (T4)-containing rat chow. This treatment produced a stable hyperthyroid state, as indicated by several biochemical/metabolic and haemodynamic parameters. Preparations of small mesenteric arteries were mounted in an isometric wire myograph. Subsequently, concentration-effect curves were determined for isoproterenol, noradrenaline and salbutamol as well as for forskolin, dibutyryl-cAMP and theophylline. We also determined concentration-effect curves to the β-adrenoceptor agonists in the presence of ICI 118,551 and CGP 20712A (i.e., in the presence of a selective β2- and β1-adrenoceptor antagonist, respectively). Apparent pA2-values were calculated to determine which β-adrenoceptor subtype causes vasodilation. These experiments indicate that β-adrenoceptor-mediated vasodilation involves both β1- and β2-adrenoceptors in mesenteric resistance vessels of both hyperthyroid and control rats. In our experiments hyperthyroidism has a sensitizing influence on vascular responses induced by the β-adrenoceptor agonist isoproterenol and the selective β2-adrenoceptor agonist salbutamol. Sensitization to isoproterenol was abolished in the presence of ICI 118,551, whereas it was emphasized in the presence of CGP 20712A. Although this was not fully supported by the results obtained with noradrenaline, these results indicate that the sensitization to β-adrenoceptor agonists is probably limited to the β2-adrenoceptor/G-protein complex and not associated with alterations of the corresponding second messenger system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00261441
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  • 8
    Electronic Resource
    Electronic Resource
    The influence of hyperthyroidism on β-adrenoceptor-mediated relaxation of isolated small mesenteric arteries (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 438-444 
    Details
    ISSN: 1432-1912
    Keywords: Key words Mesenteric resistance arteries ; Hyperthyroidism ; β-adrenoceptor agonists ; β2-adrenoceptor ; Second messenger system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We investigated the influence of hyperthyroidism on relaxant responses of small mesenteric resistance arteries to β-adrenoceptor agonists and to compounds stimulating the corresponding second-messenger system. Hyperthyroidism was induced by feeding rats for 28 days with 5 mg/kg L-thyroxine (T4)-containing rat chow. This treatment produced a stable hyperthyroid state, as indicated by several biochemical/metabolic and haemodynamic parameters. Preparations of small mesenteric arteries were mounted in an isometric wire myograph. Subsequently, concentration-effect curves were determined for isoproterenol, noradrenaline and salbutamol as well as for forskolin, dibutyryl-cAMP and theophylline. We also determined concentration-effect curves to the β-adrenoceptor agonists in the presence of ICI 118,551 and CGP 20712A (i.e., in the presence of a selective β2- and β1-adrenoceptor antagonist, respectively). Apparent pA2-values were calculated to determine which β-adrenoceptor subtype causes vasodilation. These experiments indicate that β-adrenoceptor-mediated vasodilation involves both β1- and β2-adrenoceptors in mesenteric resistance vessels of both hyperthyroid and control rats. In our experiments hyperthyroidism has a sensitizing influence on vascular responses induced by the β-adrenoceptor agonist isoproterenol and the selective β2-adrenoceptor agonist salbutamol. Sensitization to isoproterenol was abolished in the presence of ICI 118,551, whereas it was emphasized in the presence of CGP 20712A. Although this was not fully supported by the results obtained with noradrenaline, these results indicate that the sensitization to β-adrenoceptor agonists is probably limited to the β2-adrenoceptor/G-protein complex and not associated with alterations of the corresponding second messenger system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00261441
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  • 9
    Electronic Resource
    Electronic Resource
    Inhibitory effect of dithiothreitol on angiotensin II-induced contractions mediated by AT1-receptors in rat portal vein and rabbit aorta (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 538-542 
    Details
    ISSN: 1432-1912
    Keywords: AT1-receptors ; Angiotensin II ; Dithiothreitol ; Losartan ; Rat portal vein ; Rabbit aorta
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The disulfide-reducing agent dithiothreitol (DTT) has been shown to reduce angiotensin II (Ang II) subtype 1 receptor (AT,) binding sites in various tissues. Its effect on Ang II-induced contractions was studied in the rat portal vein and rabbit aorta. In the isolated rat portal vein, DTT shifted the concentration-response curve for Ang II to the right (DTT 0.5–3 mmol/l) and depressed the maximal response (DTT 1–3 mmol/l). DTT 5 mmol/l almost abolished the effect of Ang II. In the isolated rabbit aorta, the inhibitory effect of DTT was more pronounced and its pattern of effect was different,since DTT 0.3 and 0.5 mmol/l caused a progressive flattening of the concentration-response curve of Ang II. DTT (1 mmol/l) fully suppressed the effect of Ang II. A biphasic curve consisting of a high sensitivity component and a component of low sensitivity for Ang II was observed after pretreatment with DTT 1 mmol/l in the rat portal vein but not in the rabbit aorta. In the presence of DTT 1 mmol/l, the AT1-receptor antagonist losartan antagonized the high sensitivity response to Ang II in a competitive manner with a pA2 value very similar to that obtained in the absence of DTT, suggesting that this response to Ang II is mediated by those AT1-receptors which were not inactivated by DTT The biphasic curve may be explained by the occurrence of a single AT1-receptor subtype existing in two different states. Another possibility might be the involvement of two AT1-receptor subpopulations. It is concluded that disulfide bonds are critical for the functional role of AT1-receptors in Ang II-induced contractions in the rat portal vein and rabbit aorta.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169144
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  • 10
    Electronic Resource
    Electronic Resource
    Calcium dependency of the AT1-receptor mediated effects in the rat portal vein: influence of calcium antagonists (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 437-442 
    Details
    ISSN: 1432-1912
    Keywords: Ang II ; AT1-receptor ; Calcium ions ; Calcium antagonists ; Rat portal vein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The calcium dependency of AT1-receptor mediated contractions was studied in isolated rat portal vein preparations. The spontaneous phasic contractile force of the rat portal vein was increased (ED50 = 1.76 mmol/l) and the frequency of contractions decreased by raising the extracellular calcium concentration. The Ang 11-induced rise in phasic contractile force (mediated by AT1-receptors, Zhang et al. 1993) proved most pronounced at 0.9 mmol/l of calcium chloride, but it was weaker at either lower or higher calcium concentrations. The maximal increases in the phasic contractile force induced by Ang II were 2.4±0.4, 14.8±0.9 and 5±0.5 mN at calcium concentrations of 0.5, 0.9 and 2.5 mmol/l, respectively. Calcium antagonists reduced at the lower and abolished at the higher concentrations (nifedipine 2×10−8 or 10−7 mol/l; verapamil 10−7 or 5 × 10−7 mol/l; diltiazem 3 × 10−7 or 10–6 mol/l) the spontaneous contractile force. All of these calcium antagonists caused a strong inhibition or suppression of the phasic contractions induced by Ang II.The rank order of potency was nifedipine 〉verapamil 〉 diltiazem. Ang II (10−6 mol/l) elicited a tonic contraction which was abolished by the AT1-receptor antagonist losartan 10-6 mol/l but not by the AT2-receptor antagonist PD 123177 (10–5 mol/l). Very high concentrations of nifedipine (10–6 mol/l), verapamil (5 × 10-6 mol/l) and diltiazem (5 × 10−6 mol/l) almost suppressed the tonic effect evoked by the activation of AT1-receptors. In a nominally Ca2+ “free”, EGTA-containing solution, a single supra-maximal concentration of Ang II (10−6 mol/l) caused a transient contraction, also mediated by AT1-receptors. This finding suggests the existence of Ang II-sensitive intracellular calcium stores in this preparation. The depletion of such stores proved complete after 4–6 min of perfusion in a Ca2+ “free”, EGTA-containing solution. In conclusion, various types of contractions (a transient contraction in a Ca2+-“free” medium, phasic and tonic contractions) induced by Ang II in the rat portal vein proved to be mediated by AT1-receptors. These contractions were clearly modified by changes in the availability of extra- and possibly intracellular calcium ions. The calcium movements elicited by stimulation of AT1-receptors in a calcium containing solution were inhibited by the three calcium antagonists investigated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170892
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