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  • 1
    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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  • 2
    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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  • 3
    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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    Paper (German National Licenses)
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