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PubMed1976

Evidence for the existence of different receptor sites for algesic agents at the endings of muscular group IV afferent units.

The hypothesis that different receptor sites for algesic agents exist at free nerve endings in skeletal muscle has been tested by administering bradykinin and 5-hydroxytryptamine (5-HT) repeatedly in anaesthetized cats and evaluating the response behaviour of single group IV afferent units from the gastrocnemius-soleus muscle. Repeated intraarterial administration of bradykinin at intervals of 1 and 2 min usually elicited fibre responses without tachyphylaxis. Injections of equieffective doses of 5-HT, however, given in the same manner evoked fibre reactions that were strongly tachyphylactic. In units responding to both bradykinin and 5-HT a refractoriness to 5-HT could be induced by repeated injections of this agent without impairing the stimulating potency of bradykinin on the same nerve ending. Such a lack of cross-tachyphylaxis seems to apply also to the effects of histamine on one side and bradykinin or 5-HT on the other. These findings suggest that bradykinin, 5-HT and probably histamine exert their excitatory action on muscular group IV afferent units via different receptor sites.

Animals↗
PubMed1976

[Reversal of the pressor effect of PGF2alpha in the rat (author's transl)].

In normal rats, prostaglandin F2alpha is a potent vasoconstrictor. The corresponding systemic hypertension is progressively attenuated by tachyphylaxis, revealing a longlasting fall of blood pressure. Tachyphylaxis is accelerated by previous injection of arachidonic acid and bradyskinin. The vasodepressive activity of PGF2alpha is inhibited by indomethacin.

Animals↗
PubMed1979

A comparative study with impromidine (SKF 92676), a potent agonist for histamine H2-receptors.

Histamine, dimaprit and impromidine caused a relaxation on the isolated cat tracheal muscle contracted by acetylcholine or serotonin. Mepyramine partially inhibited the relaxing effect of histamine without altering that of impromidine and dimaprit. Both impromidine and dimaprit produced a dose-dependent fall in perfusion pressure of the isolated perfused guinea-pig lung while histamine has a pressor effect in this preparation which reversed into a depressor one in the presence of mepyramine. Both dimaprit and impromidine also produced a fall in perfusion pressure and urine flow of the isolated perfused rabbit kidney. A rapid tachyphylaxis developed to the effect of impromidine in the kidney but not to dimaprit. A cross-tachyphylaxis was also observed between impromidine and dimaprit. The agonistic potency of impromidine was found to be very much higher than histamine and dimaprit. Metiamide has a competitive inhibitory effect against impromidine and dimaprit on the isolated perfused lung, kidney and tracheal muscle. It was concluded that impromidine is a very potent pure histamine H2-receptor agonist when compared with histamine and dimaprit on the investigated tissues.

Airway Resistance↗
PubMed1976

Effect of premedication of coenzyme Q10 on pancreozymin-induced pancreatic secretion in rats.

Effect of Coenzyme Q10 (CoQ10), an essential coenzyme in oxidative phosphorylation in the mitochondria, was studied in the rat's pancreas. A dose of pancreozymin (0.2 u/100 g body wt) was injected into the femoral vein at 20 min intervals. The initial injection produced a definite increase in amylase output and the pancreatic juice flow. Subsequent injections, however, caused smaller responses than the preceding (tachyphylaxis). When CoQ10 (3 mg/100 g body wt) had been administrated 1 hour prior to the initial stimulation, both the amylase output and the rate of juice flow were significantly enhanced: the tachyphylaxis almost disappeared. Effect of CoQ10 was also observed in the isolated and perfused pancreas. CoQ10 produced slight increase in pancreozymin-induced amylase output, but the increase was not significant. The effect of CoQ10, to increase the pancreatic blood flow, seems to be involved in the in situ effect of CoQ10 in cooperation with the direct effect on pancreatic acinar cells.

Amylases↗
PubMed1975

Sodium nitroprusside in children: Observations on metabolism during normal and abnormal responses.

Three different responses to sodium nitroprusside as a hypotensive agent during anaesthesia in children are described. A constant high dose (greater than 3 mg/Kg) response to, abnormal resistance to and tachyphylaxis to the drug are recognised and are dangerous and potentially lethal. They are probably related to abnormalities of cyanide-thiocyanate metabolism resulting in cyanide accumulation. The abnormal responses produce metabolic acidosis, an increase in mixed venous oxygen tension and a decrease in arterial mixed venous oxygen content difference. Tachyphylaxis may be due to depletion of endogenous thiosulphate and was reversible by sodium thiosulphate therapy (150 mgm/Kg) in two cases in which it was used.

Adolescent↗
PubMed1983

RHC 3288 [1-methyl-2(1,3,4-oxadiazol-2(3H)-one-5-yl) benzimidazole] and related compounds. Novel inhibitors of histamine release from rat mast cells and human basophils.

RHC 3288 [1-methyl-2(1,3,4-oxadiazol-2(3H)-one-5-yl) benzimidazole] and twenty-five related 5-substituted oxadiazolones have been investigated for their antiallergic activities in three in vitro models of anaphylaxis. Sixteen compounds were potent (I50 less than or equal to 50 microM) inhibitors of antigen-induced release of histamine (AIR) from rat mast cells (RMC), and seven compounds inhibited anti-IgE-induced release of histamine from human basophils (I50 less than or equal to 100 microM). The antiallergic activity profiles of RHC 3288 and three other compounds in these models have been compared with that of disodium cromoglycate (DSCG). As inhibitors of AIR from RMC, RHC 3288, 3334, 3354 and 3380 were 3 to 10 times more potent than DSCG. In the same model (AIR from RMC), activity profiles of all four RHC compounds were identical to that of DSCG in the following respects: loss of inhibitory activity with increasing preincubation time, tachyphylaxis and cross-tachyphylaxis to each other, and inability to inhibit histamine release stimulated by Ca2+ ionophore, dextran + phosphatidyl serine and compound 48/80. RHC 3288, 3334, 3354 and DSCG had no effect in the other two models, histamine release from guinea pig lung mediated predominantly by IgG1 class of antibodies and anti-IgE-induced histamine release from human basophils. We conclude that RHC 3288 is a potent inhibitor of mediator release with a mechanism of action similar to that of DSCG.

Animals↗
PubMed1987

REV 2871 (CHBZ): a potent antiallergic agent with a novel mechanism of action. I. Activity profile as an inhibitor of mediator release.

REV 2871 (CHBZ) and its putative metabolite REV 3579-Z (also designated in the literature as RHC 3579-Z) were shown to be potent and orally effective inhibitors of passive cutaneous anaphylaxis (PCA) in the rat (ED50 = 12 mg/kg). The activity profiles of CHBZ, REV 3579-Z and disodium cromoglycate (DSCG) were compared as inhibitors of histamine release (HR) in vitro from rat mast cells, human basophils, and guinea pig lung slices. CHBZ was a potent inhibitor of both immunologic and non-immunologic HR (I50 2-20 microM from rat mast cells). The activity profile of CHBZ as an inhibitor of HR from rat mast cells differed from that of DSCG and REV 3579-Z in the following respects: increasing inhibition of HR with increasing preincubation time; irreversibility of the inhibition; lack of tachyphylaxis and cross-tachyphylaxis to DSCG; potentiation of the inhibition of antigen-induced release of histamine (AIR) by DSCG; and inhibition of HR induced by dextran + phosphatidyl serine, compound 48/80, ionophore A23187 and platelet activating factor (PAF). In the human basophil model, CHBZ was: a potent inhibitor (I50 = 25 microM) of anti-IgE-induced release (AbIR), whereas DSCG and REV 3579-Z had no effect on AbIR; more potent as an inhibitor of AbIR than ionophore-induced release, whereas the reverse was true for proxicromil; an inhibitor of PAF-induced release, whereas proximcromil stimulated it; and potentiative with proxicromil for inhibition of AbIR. In the guinea pig lung slice model, CHBZ inhibited AIR (I50 = 800 microM) whereas DSCG and REV 3579-Z did not (I50 greater than 300 microM). We conclude that CHBZ is an orally effective antiallergic agent whose mechanism of action as an inhibitor of mediator release is different from DSCG and proxicromil.

Animals↗
PubMed1982

Do mast cell degranulators release prostaglandins from frog atria?

Isolated atria of frogs responded to compound 48/80 and d-tubocurarine with a delayed stimulation that showed tachyphylaxis and cross-tachyphylaxis indicating a common indirect mechanism. The blockers of H2-histamine, serotonin and beta-adrenergic receptors did not significantly antagonise these responses. However, in experiments with ex vivo and in vitro indomethacin-treated atria, the stimulant effects of mast cell degranulators were not observed, indicating a possible involvement of the prostaglandins.

Animals↗
PubMed1982

Response of the guinea-pig urinary bladder to purine and pyrimidine nucleotides.

The ability of purines and pyrimidines to cause and inhibit contractile responses was examined in strips of guinea-pig urinary bladder. Adenosine 5'-triphosphate (ATP), beta, gamma-methylene ATP (APPCP), adenosine 5'-diphosphate (ADP), guanosine 5'-triphosphate (GTP) and cytidine 5'-triphosphate (CTP) caused concentration-dependent contractions of the bladder. The order of potency was APPCP greater than ATP greater than GTP=CTP greater than ADP. Adenosine 5'-monophosphate, adenosine, guanosine 5'-diphosphate, guanosine 5'-monophosphate, guanosine, cytidine 5'-diphosphate, cytidine 5'-monophosphate, adenosine, guanosine 5'-diphosphate, guanosine 5'-monophosphate, guanosine, cytidine 5'-diphosphate, cytidine 5'-monophosphate and cytidine had no apparent contractile activity up to 10(-3) M. Cumulative administrations of 5 X 10(-4) M APPCP, ATP, ADP, GTP or CTP resulted in complex desensitization of the tissue to the contractile activity of the nucleotide. Tissues desensitized to GTP or CTP were non-responsive to ATP suggesting cross-tachyphylaxis. Nucleotides lacking contractile activity or nucleosides did not alter the response of the bladder to ATP; except AMP and adenosine which significantly reduced the contraction. These results suggest that the polyphosphate structure, and not the base, is the determining portion of the nucleotide for promoting contractile activity and the development of tachyphylaxis.

Animals↗
PubMed1989

Effect of capsaicin on gastric corpus smooth muscle of the rat in vitro.

Circular strips of the rat gastric corpus muscle were mounted in Krebs solution for isometric tension recording. Addition of capsaicin usually led to either relaxation or contraction, but in some strips a biphasic response was observed. Although no clear-cut concentration-response relationship could be established, capsaicin predominantly induced contraction at 500 nM, whereas at 5 microM it mainly induced relaxation. In Krebs solution containing atropine plus guanethidine, the contraction induced by 500 nM capsaicin was significantly reduced. The contraction induced by capsaicin was abolished by spantide, a tachykinin antagonist, or by tachyphylaxis to substance P. Calcitonin gene-related peptide relaxed gastric smooth muscle, however, a dose-response relationship could not be established. This peptide contracted the muscle strips only at 1 microM. Tachyphylaxis to calcitonin gene-related peptide did not significantly influence the action of capsaicin. Vasoactive intestinal polypeptide dose dependently relaxed gastric corpus strips; however, these responses were qualitatively different from those to capsaicin. It is concluded that capsaicin contracts rat gastric smooth muscle via the release of tachykinins; cholinergic interneurones are involved. The mediator of the capsaicin-induced relaxation has yet to be determined.

Animals↗
PubMed1993

Vasoconstrictor reaction to prostaglandins E1 and E2 in the isolated rat hindlimb mediated through serotonin release.

The vasoconstrictor effects of prostaglandins E (PGEs) were studied in the isolated perfused hindlimbs of the rat. Doses of PGE1 in the range of 0.01-10 micrograms caused dose-dependent increases in perfusion pressure with rapid development of tachyphylaxis. The pressure increases were inversely temperature-dependent, being 4.8 +/- 1.2 mm Hg at 37 degrees C and 22.2 +/- 1.8 mm Hg at 27 degrees C. The vasoconstriction was limited to PGE1 and PGE2. Other prostaglandins tested, PGF2 alpha, PGD2, PGA1, 7-oxo-PGI2 and arachidonic acid, were without any effect at 27 degrees C. Increased serotonin concentrations were found in the effluent after the administration of 1 microgram of PGE1. The pressor response to PGE1 was blocked by 5-HT2 antagonists, ketanserin (2 micrograms) and naftidrofuryl (100 micrograms), while the alpha-adrenoceptor antagonist phentolamine (6.7 micrograms) was without effect. Rapid tachyphylaxis of the development of vasoconstriction was observed after the repeated administration of PGE1 and PGE2. PGE1 (1 microgram) induced desensitization with more than 60 min duration. All the findings suggest that serotonin was liberated in the rat hindlimbs by PGEs.

Adrenergic alpha-Antagonists↗
PubMed1994

Cardiovascular effects of different schedules of nicotine administration on spinal rats: influence of pentobarbital.

This work examined the cardiovascular effects of different schedules of i.v. nicotine administration with respect to doses and timing in non-anesthetized and pentobarbital-treated spinal rats. For this purpose, complete nicotine dose-response curves were made for mean arterial pressure and heart rate. In non-anesthetized spinal rats, tachyphylaxis was not found for the pressor effects; moreover, consecutive doses, given at short intervals, produced additive actions. Furthermore, nicotine produced a biphasic heart rate response: an initial and brief bradycardia followed by a longer lasting tachycardia. In pentobarbital-treated rats, the sensitivity of the cardiovascular system to nicotine was decreased; in these rats, consecutive nicotine doses did show tachyphylaxis for the pressor and tachycardiac responses. The present series of experiments, using different schedules of administration for single and consecutive nicotine doses, demonstrated opposite tachyphylactic effects in non-anesthetized and in pentobarbital-treated spinal rats.

Animals↗
PubMed1989

Peptide histidine isoleucine and vasoactive intestinal polypeptide cause relaxation of opossum internal anal sphincter via two distinct receptors.

The purpose of this investigation was to characterize the nature of peptide histidine isoleucine (PHI) and vasoactive intestinal polypeptide (VIP) receptors, and to examine the role of PHI in internal anal sphincter (IAS) relaxation. The studies were performed on opossums anesthetized with alpha-chloralose. The pressures in the IAS were recorded using continuously perfused catheters. The IAS responses to PHI analogues, PHI-27, PHM-27, PHI-(14-27)-NH2, PHI-(1-13), to VIP, to rectal balloon distention, sacral nerve stimulation, and local intramural stimulation were evaluated before and after PHI-(14-27)-NH2, PHI tachyphylaxis, and the VIP antagonists [4 Cl-D-Phe6, Leu17] VIP (VIP analogue) and (N-Ac-Tyr1, D-Phe2)-GRF(1-29)-NH2 (growth hormone releasing factor analogue). The inhibitory responses by all of the PHI analogues and VIP were not modified by tetrodotoxin. PHI-(14-27)-NH2 and PHI tachyphylaxis caused significant antagonism of the fall in internal anal sphincter pressure by PHI-27 and PHM-27 without modifying the IAS responses to VIP and rectal balloon distention, sacral nerve stimulation, and local intramural stimulation. On the other hand, VIP and growth hormone releasing factor analogues caused significant antagonism of VIP responses without modifying the responses to PHI-27. We conclude that distinct PHI and VIP receptors are present in the IAS smooth muscle and that PHI may not play a significant role in the IAS relaxation via the rectoanal reflex.

Anal Canal↗
PubMed1991

Erythromycin acts through a cholinergic pathway to improve canine-delayed gastric emptying following vagotomy and Roux-Y antrectomy.

We have demonstrated that erythromycin improves gastric emptying in dogs following truncal vagotomy and Roux-en-Y antrectomy (VRYA). To explore its mechanism of action we studied gastric emptying and myoelectric activity in a canine Roux model and administered atropine simultaneously with erythromycin. Tachyphylaxis was evaluated following short-term administration. Four dogs with delayed gastric emptying following VRYA were studied. Radionuclide solid gastric emptying was measured, with simultaneous myoelectric recordings obtained from the duodenum and Roux limb. Study groups were: (1) saline control (VRYA dogs); (2) erythromycin 1 mg/kg iv over 1 hr; (3) erythromycin 3 mg/kg po tid for 1 week, with repeat studies using erythromycin 1 mg/kg iv over 1 hr; and (4) atropine 0.5 mg/kg iv bolus, followed by a 1-hr infusion of atropine 0.05 mg/kg and erythromycin 1 mg/kg. Control Roux animals had severe gastric retention (73 +/- 5% at 2 hr, compared to 27 +/- 6% following iv erythromycin (P less than 0.01). Clustered spike bursts were observed in the Roux limb following erythromycin. Atropine abolished the gastrokinetic response and suppressed the myoelectric response to erythromycin (81 +/- 3% retention at 2 hr, P less than 0.01 compared to erythromycin alone). The response to erythromycin was unchanged after 1 week of tid administration (40 +/- 14% retention at 2 hr postprandial, P = NS). Erythromycin improves gastric emptying in VRYA dogs via a cholinergic pathway and does not exhibit tachyphylaxis following short-term administration.

Anastomosis, Roux-en-Y↗
PubMed1995

Agmatine: a novel endogenous vasodilator substance.

The purpose of the study was to investigate the effects of agmatine, an endogenous clonidine-displacing substance (CDS), on systemic hemodynamics in the anesthetized rat. Bolus intravenous (i.v.) injections of agmatine decreased systemic arterial pressure (SAP) and systemic vascular resistance in a dose-dependent manner. The development of acute tachyphylaxis to the systemic vasodepressor response to agmatine did not induce cross-tachyphylaxis to the systemic vasodepressor responses to bradykinin, isoproterenol and nitroglycerin. The present data demonstrate agmatine, as a CDS and agonist for imidazoline (I) receptors, possesses marked systemic vasodilator activity in the rat. The present data suggest that activation of I receptors may represent a novel mechanism of vasodilation in vivo.

Agmatine↗
PubMed1986

Effects of chronic morphine treatment on opioid-induced inhibition and facilitation of acetylcholine release in guinea-pig thalamic slices.

The effect of chronic morphine treatment on acetylcholine (ACh) release from guinea-pig thalamic slices and on [3H]-dihydro-morphine binding to the brain of normal, tolerant and abstinent guinea-pigs was studied. Morphine (30 microM) inhibited the electrically-evoked ACh release to the same extent in normal and tolerant slices. This effect was antagonized by naloxone. Morphine (30 microM) in the presence of naloxone (10 microM) facilitated electrically-evoked release of ACh. This effect displayed tachyphylaxis in normal slices and was absent in the brain taken from tolerant animals. The reduction of [Ca++] in the medium increased the facilitatory response in normal slices and the inhibitory response in normal and tolerant tissue. The high and low affinity binding sites to [3H]-dihydro-morphine were the same in the thalami, caudate nuclei and cortices of normal, tolerant and abstinent animals. It is concluded that the cholinergic structures of the guinea-pig thalamus are unlikely to be involved in morphine tolerance. In fact, the facilitation appears to be an ancillary phenomenon which quickly displays tachyphylaxis in normal tissue while the inhibition of ACh release remains unchanged.

Acetylcholine↗
PubMed1992

Blood pressure changes and sympathetic function in rats given cyclohexylamine by intravenous infusion.

Intravenous infusion of cyclohexylamine (30-120 mg/kg) caused a dose-dependent increase in blood pressure in urethane-anesthetized rats. The increase in blood pressure was inversely related to the duration of the infusion. The blood pressure returned to baseline values (+/- 5 mm Hg) within 60 min of the end of the infusion after doses of 30 and 60 mg/kg were administered over 20 and 40 min. The plasma concentrations of cyclohexylamine were related linearly to the administered dose and decreased only 27% between the end of the infusion and 60 min later. The concentration-effect relationship showed clockwise hysteresis, indicative of tachyphylaxis, as has been reported in humans (Eichelbaum et al., 1974). Administration of bolus doses of tyramine at the end of the infusion or 60 min later demonstrated the presence of an indirect sympathomimetic response, although this was attenuated to a greater extent by high doses and more rapid infusions of cyclohexylamine. An almost complete loss of response to tyramine was found only in animals given 120 mg/kg over 40 min. The presence of a tyramine response 60 min after the infusion of 60 mg/kg occurred when there was an essentially complete reversal of the hypertensive effect of cyclohexylamine. These data indicate that the hypertensive effect of the indirectly acting sympathomimetic amine cyclohexylamine occurs primarily during rapid increases in plasma concentrations. Tachyphylaxis develops rapidly after the cessation of the infusion which is probably due largely to reuptake of released noradrenaline at low doses and depletion of releasable noradrenaline at high doses.

Animals↗
PubMed1984

Effect of the purified phospholipases A2 from snake and bee venoms on rabbit platelet function.

Effects of seven purified phospholipases A2 from the venoms of snakes (Naja naja atra, Trimeresurus mucrosquamatus and T. gramineus) and honey bee (Apis mellifera) on rabbit washed platelet suspension in the absence of bovine serum albumin have been studied. Only phospholipases A2 from N. n. atra, T. mucrosquamatus and A. mellifera venoms induced platelet aggregation with small amounts of 14C-serotonin release. They showed tachyphylaxis and also cross-tachyphylaxis in inducing platelet aggregation. The former two phospholipases A2 exhibited biphasic responses in which irreversible aggregations appeared at concentrations of 1-10 micrograms/ml. At higher concentrations, they elicited the reversible aggregation. Exogenous Ca2+ was essential to their activity. Indomethacin and EDTA completely abolished both phospholipase A2 induced platelet shape change and aggregation, while mepacrine, prostaglandin E1, verapamil and nitroprusside inhibited only the aggregation response. p-Bromophenacyl bromide-modified phospholipases A2, which almost completely lost enzymatic activity, failed to induce platelet aggregation. Phosphatidylcholine, phosphatidylethanolamine and phosphatidylinositol inhibited the phospholipase A2-induced platelet aggregation. These phospholipases A2 induced thromboxane B2 formation which was inhibited by EDTA and indomethacin, but not by prostaglandin E1. Pre-treatment of platelet suspension with phospholipase A2 from N. n. atra or A. mellifera venom (50 micrograms/ml) inhibited platelet aggregation induced by sodium arachidonate or collagen, but not that induced by thrombin or ionophore A-23187. Exogenous sodium arachidonate or lysophosphatidylcholine also showed unaltered inhibitory spectrum on platelet aggregation. It is concluded that phospholipases A2 induce platelet aggregation by virtue of their enzymatic activity, cleaving the membrane phospholipids resulting in arachidonic acid release and formation of thromboxane A2. On the other hand, the cleaved products, lysophosphatidylcholine, arachidonic acid or arachidonate metabolites (via lipoxygenase pathway) may be responsible for anti-platelet activity.

Animals↗