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5-HT caused concentration-dependent relaxation of methoxamine contracted cat isolated saphenous vein and atropine pretreated guinea-pig isolated ileum contracted with histamine. The concentration required to cause 50% of its maximum effect was 7.4 X 10(-7) and 1.4 X 10(-6) mol/l respectively. alpha-Methyl 5-HT was at least 200 times weaker than 5-HT in this respect. The relaxant action of 5-HT in both preparations was not antagonised by atropine, indomethacin, cimetidine, propranolol or tetrodotoxin. In both preparations the relaxant effect was not specifically antagonised by cyproheptadine but was specifically and competitively antagonised by methysergide (pA2 values of 6.75 and 7.37 in cat saphenous vein and guinea-pig ileum, respectively). The results suggest that the 5-HT mediated relaxation in both preparations is mediated directly via a similar 5-HT receptor. The weak antagonistic action of methysergide and lack of relaxant effects with alpha-methyl 5-HT is consistent with the view that this receptor is not a 'D' or 'M' 5-HT-receptor.
In isolated rat aorta and urinary bladder, indomethacin inhibited the synthesis of the prostaglandins (PG) PGI2, PGE2, PGF2 alpha and TXA2 equipotently when PG synthesis was stimulated with excitatory receptor agonists (noradrenaline and carbachol), fluoride (a G protein activator), phorbol ester (a protein kinase C (PKC) activator) and calcium ionophore A23187 (a creator of artificial calcium channels). However, there was a marked right shift (30 fold) in the indomethacin concentration-inhibition curves when PG synthesis was stimulated by arachidonate (PG substrate) and trauma (freeze fracturing and sonication). Although less potent than indomethacin, the NSAIDs tiaprofenic acid and ibuprofen showed a similar disparity between the IC50s with the same PG stimulators. Since PG synthesis stimulated by receptor agonists, fluoride, phorbol ester and A23187 is dependent on calcium channel activation whereas trauma and arachidonate-stimulated PG synthesis bypass calcium channel activation, these data indicate that NSAIDs inhibit not only cyclooxygenase but also (and more potently) the mobilisation of Ca2+ linked to PG synthesis in these tissues.
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Calcium ions produce a 3-4-fold stimulation of the actin-activated ATPase activities of phosphorylated myosin from bovine pulmonary artery or chicken gizzard at 37 degrees C and at physiological ionic strengths, 0.12-0.16 M. Actins from either chicken gizzard or rabbit skeletal muscle stimulate the activity of phosphorylated myosin in a Ca2+-dependent manner, indicating that the Ca2+ sensitivity involves myosin or a protein associated with it. Partial loss of Ca2+ sensitivity upon treatment of phosphorylated gizzard myosin with low concentrations of chymotrypsin and the lack of any change on similar treatment of actin supports the above conclusion. Although both actins enhance ATPase activity, activation by gizzard actin exhibits Ca2+ dependence at higher temperatures or lower ionic strengths than does activation by skeletal muscle actin. The Ca2+ dependence of the activity of phosphorylated heavy meromyosin is about half that of myosin and is affected differently by temperature, ionic strength and Mg2+, being independent of temperature and optimal at lower concentrations of NaCl. Raising the concentration of Mg2+ above 2-3 mM inhibits the activity of heavy meromyosin but stimulates that of myosin, indicating that Mg2+ and Ca2+ activate myosin at different binding sites.
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1. Dose-response curves for angiotensins II and III in the rat isolated uterus, portal vein and aorta, in the absence and presence of the antagonist [Sar1Ile8]ANG II, have been analyzed by methods which detect cooperativity. 2. Hanes-Woolf transformations of dose-response data were used to define phases of positive homotropic cooperativity, and this information was applied to the interpretation of Hill plots. 3. The level of positive cooperativity was found to be higher for ANG II (nH = 1.35-2.00) than ANG III (nH = 1.02-1.43) in the three tissues studied. 4. In the presence of the antagonist [Sar1Ile8]ANG II a decrease in the level of cooperativity produced by both agonists was observed, and high concentrations of the antagonist could induce negative cooperativity. 5. These findings have been interpreted on the basis of a 2-site agonist binding mechanism involving receptor dimers, in which angiotensin agonists induce an increase in their own receptor binding affinity, whereas the antagonist [Sar1Ile8]ANG II decreases the affinity of angiotensin receptors for ANG II and ANG III.
1. Trandolaprilat was found to inhibit angiotensin I (Ang I)-induced contraction of the rat thoracic aorta, and to augment bradykinin(BK)-induced contraction of the guinea pig ileum. In inhibitory activity (IC50) on the Ang I induced contraction of the rat thoracic aorta, trandolaprilat was about 2.4 times as potent as enalaprilat. Concerning the augmenting activity (AC50) on bradykinin-induced contraction of the guinea pig ileum, the activity of trandolaprilat was similar to that of enalaprilat. 2. Trandolaprilat had no effect on contractions induced by norepinephrine, PGF2 alpha, 5-HT or CaCl2 in the thoracic aorta of rats. 3. Trandolaprilat produced endothelium-dependent relaxation. This relaxation was inhibited by NG-methyl-L-arginine treatment, suggesting that endothelium-dependent relaxation of trandolaprilat is related to endothelium-derived-relaxation-factor(EDRF/NO). Like trandolaprilat, captopril also produced endothelium-dependent relaxation, whereas enalaprilat had no effect.
The effects of an aqueous extract of Ferula ovina were tested in vitro using isolated segments of rabbit and guinea pig intestine, trachea and aorta. The extract inhibited the spontaneous movements of rabbit jejunum and guinea pig ileum and the contractions induced by acetylcholine. The aqueous extract also inhibited the contractions of rabbit trachealis muscle induced by acetylcholine and the contractions of guinea pig trachealis muscle induced by histamine. These inhibitions were dose-dependent and reversible. However, the aqueous extract did not inhibit the contractions of rabbit and guinea pig aortic rings induced by norepinephrine. These data suggest that this plant has non-specific anticholinergic and antihistaminic antispasmodic effects.
Calcium store of the skinned fibers of the guinea-pig portal vein, pulmonary artery and taenia caeci consisted of two classes: one with both Ca-induced Ca release (CICR) and inositol 1,4,5-trisphosphate (IP3)-induced Ca release (IICR) mechanisms (S alpha) and the other only with IICR mechanisms (S beta). Ryanodine, applied during the CICR was activated, locked the CICR channels open, but the drug had practically no effect on the IICR mechanism. Thus, after the ryanodine treatment the Ca store with the CICR (S alpha) lost its capacity to hold Ca. Changes in the agonist-evoked contraction of intact muscle due to the ryanodine treatment suggest that agonists release Ca from S alpha which produces the initial phase of contractures.
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