SEARCH · PubMed Health

Results for “Tachyphylaxis”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1978

Characteristics and tachyphylaxis of gastrin-stimulated gastric acid secretion in the cat.

1. The characteristics of gastrin-stimulated gastric acid secretion were investigated in conscious cats fitted with chronic cannulated gastric fistulae, with particular reference to tachyphylaxis. 2. There is a significant postive correlation between the peak acid secretion in response to pentagastrin 8 microgram kg-1 hr-1 and body weight. Male cats secret significantly greater amounts of acid in response to pentagastrin than females. The difference is lessened, but not eliminated, by expressing the acid out put in terms of body weight. 3. Pentagastrin stimulates a dose-dependent increase in acid secretion in the range 0.5-32 microgram kg-1 hr-1 when the response to each dose is assayed on separate occasions. Pentagastrin 64 microgram kg-1 hr-1 does not produce a further increase in acid secretion. The acid response to pentagastrin 1-16 microgram kg-1 hr-1 assayed on a single occasion by a continuous infusion method shows a dose-response relationship up to 8 microgram kg-1 hr-1 when it reaches a plateau of secretion. There is no difference between the two methods of assaying the gastric acid stimulating activity using doses of pentagastrin up to 8 microgram kg-1 hr-1. 4 The acid secretion in response to pentagastrin 8 microgram kg-1 hr-1 reaches a maximum after 45 min of stimulation and thereafter shows tachyphylaxis. Over a period of 5 hr there are at least two phases of tachyphylaxis distinguishable. During the period 0.75--2.5 hr of stimulation there is a fast phase of tachyphylaxis (-32.0 muequivH+kg-1 15 min-1). This is followed by a slow phase of tachyphylaxis (-9.4 muequivH+kg-1 15 min-1) up to 5 hr of stimulation. 5. The absolute rate of the fast phase of tachyphylaxis of acid secretion (muequivH+kg-1 15 min-1) increases with increasing doses of pentagastrin, but rates of tachyphylaxis are similar when expressed as a percentage of the peak acid response to the particular dose of pentagastrin (5.1--7.8% 15 min-1). Synthetic human gastrin-17, the synthetic C-terminal decapeptide of human gastrin and the C-terminal tetrapeptide of gastrin have comparable rates of tachyphylaxis. The possible receptor models for the tachyphylaxis of gastrin-stimulated acid secretion are discussed.

Animals↗

PubMed1976

Further studies on angiotensin tachyphylaxis.

Rabbit aorta and rat fundus do not display tachyphylaxis to angiotensin II (Asp1)angiotensin II) at 37 degrees C. These tissues do, however, display tachyphylaxis to [Sar1]angiotensin II (N-methylglycine 1 angiotensin II) and [dimethylglycine angiotensin II, respectively, at this temperature. At 22 degrees C, both tissues displayed rapid tachyphylaxis to [Asp1]angiotensin II which was reversed on prolonged incubation in peptide-free medium. At 37 degrees C, but at a lower than normal pH (pH 6.5 instead of 7.4), the rabbit aorta developed rapid tachyphylaxis to [Asp1)angiotensin II; this effect also was reversed on prolonged incubation in peptide-free medium. The rat uterus, at 30 degrees C, displayed tachyphylaxis to [Asp1]angiotensin II and analogs in order of rate of onset: [Sar1]angiotensin II greater than [Asp1]angiotensin II greater than [des-Asp1]angiotensin II. Over half of the individual uterine strips tested displayed no tachyphylaxis to [des-Asp1]angiotensin II. However, at 22 degrees C tachyphylaxis to all three compounds was rapid on onset and was reversed on prolonged incubation. The results indicate a correlation between affinity of the peptide analog for angiotensin receptor and its ability to induce tachyphylaxis. A possible involvement of membrane-bound enzymes in the onset and duration of tachyphylaxis is suggested.

Angiotensin II↗

PubMed1979

Characteristics of histamine tachyphylaxis in canine tracheal smooth muscle.

In isolated canine tracheal smooth muscle, repeated administrations of histamine result in a rapid reduction in contractile response to about 15% of the initial contraction (tachyphylaxis). Development of this tachyphylaxis is specific inasmuch as: 1) it does not develop to acetylcholine (10(-6) M or 10(-4) M), or serotonin (10(-5) M; and 2) maximally developed histamine tachyphylaxis is not associated with a parallel reduction in response to acetylcholine. Pretreatment with propranolol (10(-5) M) or phentolamine (10(-4) M) does not prevent tachyphylaxis: however, pretreatment with atropine (10(-4) M) does prevent tachyphylaxis in about 50% of the animals tested. Tachyphylaxis to histamine can be reversed in a dose- and time-dependent fashion with prostaglandin synthesis inhibiting agents. The order of potency obtained with such compounds (indomethacin greater than mefenamic acid greater than oxyphenbutazone greater than acetylsalicylic acid) is consistent with potencies for inhibition of prostaglandin synthesis found in the literature. Also, in indomethacin pretreated strips in which tachyphylaxis to histamine was prevented, exogenous addition of PGE2 (1.42 x 10(1-) M to 2.84 x 10(-9) M) and PGA2 in a high concentration (2.9 x 10(-9) M) are capable of selectively reducing the response to histamine without an effect on acetylcholine-induced contractions. These data suggest that the mechanism of histamine tachyphylaxis in the canine tracheal smooth muscle preparation involves prostaglandin synthesis.

Acetylcholine↗

PubMed1978

The development of tachyphylaxis to electrical stimulation in guinea-pig ileal longitudinal muscles and the possible participation of adenosine and adenine nucleotides.

1 Electrically (30 Hz) induced contractions of guinea-pig isolated ileal longitudinal muscles were reduced by tetrodotoxin (1 micron), adenosine (30 micron) and morphine (10 micron). 2 When stimulated with 10 or 30 Hz for 10 s at 1 min intervals, a progressive decline of amplitude of the contraction was seen (development of tachyphylaxis). At this time, the contractile response to 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) (10 micron) was also greatly reduced. 3 The smaller responses to electrical stimulation and DMPP during tachyphylaxis were restored to their initial amplitude by the addition of theophylline (10 micron). The appearance of tachyphylaxis was prevented by pretreatment with theophylline (1 to 10 micron) and was greatly accelerated by pretreatment with dipyridamole (0.1 1 micron). 4 In [14C]-choline or [3H]-adenosine preloaded muscle strips, electrical stimulation (30 Hz) increased the 14C- or 3H-output, the effect being sensitive to tetrodotoxin blockade. The tachyphylaxis to electrical stimulation was accompanied by a considerable and sustained increase in 3H-output, an effect that was accelerated by dipyridamole (1 micron). The 14C-output initially increased but fell off gradually with the development of tachyphylaxis at which time theophylline (30 micron) reversed the fall. 5 There was a marked increase in the proportion of released [3H]-adenosine to its derivatives during the development of tachyphylaxis. Approximately 60% of the released total radioactivity after tachyphylaxis was found to be [3H]-adenosine. 6 These results suggest that the development of tachyphylaxis may be closely associated with the release of endogenous adenosine derivatives (mostly adenosine) which have presynaptic inhibitory actions on the cholinergic elements in guinea-pig ileum.

Acetylcholine↗

PubMed1977

The effects of somatostatin and metiamide on tachyphylaxis of pentagastrin stimulated gastric acid and pepsin secretion in the conscious cat.

1. Pentagastrin stimulated gastric acid and pepsin secretions show parallel rates of tachyphylaxis in the conscious cat. The responses to histamine show only slight tachyphylaxis. 2. Somatostatin 10 microng.kg(-1).hr(-1) inhibits pentagastrin but not histamine stimulated acid secretion and inhibits pentagastrin stimulated pepsin secretion. 3. The inhibition of pentagastrin stimulated acid and pepsin secretion by Somatostatin delays the tachyphylaxis of these responses, but the rates of tachyphylaxis when they do subsequently occur are identical. 4. Metiamide 10 mg-kg(-1)-hr(-1) equally inhibits histamine and pentagastrin stimulated acid secretion but does not inhibit pentagastrin stimulated pepsin secretion. 5. Inhibiton of acid secretion during metiamide infusion neither prevents nor delays acid nor pepsin tachyphylaxis. 6. It is suggested that tachyphylaxis of acid and pepsin secretion is a gastrin receptor phenomenon and that Somatostatin occupies or modifies the behaviour of these receptors, preventing tachyphylaxis. Metiamide, however, exerts its action only on the histmine H2-receptor and not the gastrin receptor mechanism, and this apparently does not prevent or delay acid tachyphylaxis.

Animals↗

PubMed1977

Requirements for angiotensin tachyphylaxis in smooth muscles.

The ability of angiotensin II (AII) and of seven N-terminally modified peptide analogs to induce tachyphylaxis in isolated preparations of the rat uterus and the guinea-pig ileum was found to correlate well with the degree of amino group protonation. No correlation was found between tachyphylaxis and the affinity for the rat uterus receptors, as measured by the reciprocals of ED50 values. Dissociation between the tachyphylactic property and receptor affinity in the rat uterus was also evident by lowering the calcium concentration in the medium, which resulted in increased tachyphylaxis without significant changes in ED50 values. In the guinea-pig ileum, tachyphylaxis correlated with the reciprocal of ED50, but there was a better correlation with amino group protonation. [6-Pyrazolylalanine] AII was approximately as tachyphylactic as AII in both smooth muscles studied, indicating that protonation of the histidine side-chain may not be important for the manifestation of tachyphylaxis. The recovery of the guinea-pig ileum for AII tachyphylaxis was not affected by repeated treatments with BaCl2, but it was partially impaired by [Suc1]AII, des-Asp-AII, bradykinin and histamine.

Angiotensin II↗

PubMed1978

Magnitude, dose-requirement and mode of development of tachyphylaxis to suxamethonium in man.

Tachyphylaxis to suxamethonium infused at a constant rate was studied in 15 surgical patients under enflurane-nitrous oxide-oxygen anaesthesia. The compound electromyographic response of the adductor pollicis muscle to stimulation of the ulnar nerve was monitored. A short-lasting and a long-lasting nearly steady state were observed in Phase I and in Phase II, respectively, during both of which a constant infusion resulted in a constant block. Tachyphylaxis occurred during the transition of phases, beginning after infusion of 1.4 +/- 0.6 (SD) mg kg-1 of suxamethonium, and 36 +/- 14 (SD) minutes of exposure. Tachyphylaxis peaked after 2.6 +/- 1.3 (SD) mg kg-1, and 72 +/- 38 (SD) minutes of exposure. The maximum gain in neuromuscular transmission from the initial maintenance level of block as the result of tachyphylaxis was 53 +/- 24 (SD) % of the control. The results are thought to reconcile previously reported conflicting clinical observations on tachyphylaxis.

Adult↗

PubMed1977

Specific desensitization (tachyphylaxis) of the guinea pig ileum to angiotensin II.

Tachyphylaxis to [Ile5]angiotensin II (angiotensin) in the isolated guinea pig ileum was found to be more severe when the Ca2+ concentration or the temperature of the medium were lowered, or when glucose was absent. Incubation with indomethacin or prostaglandin E2 did not affect the onset of tachyphylaxis or recovery from the tachyphylactic state. The angiotensin dose-response curves of tachyphylactic organs were shifted to the right, and the maximum responses were depressed in proportion to the conditioning doses of the hormone. The recovery from tachyphylaxis followed zero-order kinetics and was not affected by Ca2+ concentration or pH. The temperature dependence of the rate of recovery yielded a value of 14.6 kcal/mol for the activation energy in the physiological temperature range. It is concluded that tachyphylaxis results from the tight binding of angiotensin to superficial calcium-binding sites in the smooth muscle cell membrane. Recovery from tachyphylaxis appears to involve displacement of angiotensin by calcium in a process that is dependent on active transport.

Angiotensin II↗

PubMed1977

Further studies on the tachyphylaxis to DSCG. The effects of concentration and temperature.

The tachyphylaxis to DSCG's inhibition of anaphylactic histamine release has been demonstrated in passively sensitized rat lung fragments. The induction of tachyphylaxis appears to depend on the concentration of the drug and the length of pretreatment. Tachyphylaxis is relatively independent of the concentration of the second exposure to DSCG. The development of tachyphylaxis is highly temperature dependent; it can be prevented by cooling the tissues to 2-4 degrees C after a brief (30 sec) preincubation with DSCG. It is suggested that DSCG inhibits histamine release by binding to 'receptor' site(s). Once the site is occupied by DSCG, it is modified by a temperature-dependent process, thus losing the ability as a 'receptor' for inhibition of histamine release. The tachyphylaxis is the result of such a modification.

Animals↗

PubMedDate not supplied

On the mechanism of tachyphylaxis to histamine in guinea pig seminal vesicle.

Repeated administration of high concentrations (10 muglml and above) of histamine produce tachyphylaxis in the seminal vesicle of guinea pig. Acetylcholine partially restores the response to histamine after development of constant tachyphylactic response. No tachyphylaxis occurred (in few experiments) in which the preparation is atropinized. Prior eserinization potentiates the response to histamine. After development of tachyphylaxis to histamine, increasing doses of histamine fail to produce log dose increase in the response. The results suggest that tachyphylaxis to histamine involves, desensitization of the receptors and further, a decrease in the release of acetylcholine may also contribute to the development of tachyphylaxis.

Animals↗

PubMed1977

Tachyphylaxis to the hypotensive effect of clonidine and the possible mechanism of this action.

In cats under chloralose-urethan anaesthesia, tachyphylaxis developed to the hypotensive effect of clonidine. Development of this tachyphylaxis was slow in the case of intravenous low doses (10--20 micrograms/kg) and rapid after high doses (50 micrograms/kg). No tachyphylaxis developed to contractions of the nictitating membrane. The phenomenon resembles the tachyphyaxis seen after the application of indirect sympathomimetics. A tachyphylaxis developed to the latter agents inhibited the hypotensive action of clonidine which, after such an intervention, invariably turned into a vasopressor effect. Clonidine exhibited the same behaviour after pretreatment with cocaine, bretylium or reserpine. Infusion of noradrenaline (10 micrograms/kg/min) counteracted the tachyphylaxis. Thus, clonidine is assumed to exert its hypotensive effect in an indirect way, i.e. by interference with the metabolism of noradrenaline.

Amphetamine↗

PubMed1977

Tachyphylaxis to beta-adrenoceptor agonists in guinea pig airway smooth muscle in vivo and in vitro.

Beta-Adrenoceptor tachyphylaxis was induced by incubating spirally cut guinea pig tracheas with isoproterenol (2.4 x 10(-7) M) for 20 min. This incubation reduced the relaxant effects of catecholamines but not of dibutyryl cyclic AMP, theophylline or sodium nitrite. Tracheas incubated with norepinephrine, phosphodiesterase inhibitors or cyclic nucleotides became tachyphylactic to isoproterenol. Pretreatment with indomethacin prevented induction of tachyphylaxis. Incubation with adenosine, methoxamine or sodium nitrite did not induce beta-adrenoceptor tachyphylaxis. When we gave isoproterenol intramuscularly to guinea pigs, airway sensitivity to aerosolized histamine was unchanged but the toxicity of parenterally administered histamine was increased. A prolonged treatment with isoproterenol reduced airway sensitivity to histamine aerosols; this reduced sensitivity was reversed by indomethacin. Thus, beta-adrenoceptor tachyphylaxis may not explain increased toxicity of parenteral histamine after isoproterenol treatment. Elevated levels of cyclic AMP and an increased synthesis of prostaglandins may result in diminished response to beta-receptor stimulation.

Adrenergic beta-Agonists↗

PubMed1976

Effects of isopropylnoradrenaline on tachyphylaxis of gastrin stimulated gastric acid secretion and mucosal blood flow in the anaesthetized cat.

1. Gastric acid and mucosal blood flow responses to sustained gastrin stimulation were studied in anaesthetized cats. 2. Acid and mucosal blood flow showed identical rates of tachyphylaxis to both large (maximal) and small doses of gastrin. 3. Isopropylnoradrenaline infused either intravenously or close arterially to the stomach produced increases in blood flow unrelated to time following the peak response to large doses of gastrin, whereas increases in acid secretion appeared to be a part removal of the acid tachyphylaxis. 4. During stimulation by small doses of gastrin, isopropylnoradrenaline increased both blood flow and acid secretion above the peak responses to gastrin alone. 5. Increases in gastrin stimulated acid and mucosal blood flow were also produced by expansion of the blood volume by dextran-saline infusions. 6. The physiological significance of these findings is discussed. 7. It is concluded that tachyphylaxis of gastric acid secretion to gastrin may be a function of the primary tachyphylaxis of mucosal blood flow.

Animals↗

PubMed1975

Calcium and angiotensin tachyphylaxis in rat uterine smooth muscle.

Studies were carried out to investigate the relationship between extracellular Ca++ and the ability of a particular smooth muscle to develop tachyphylaxis to angiotensin II (AII). Stimulation of rat uterus by AII was found to be dependent on extracellular Ca++. Placing the tissue in 0 Ca++ completely blocked AII-induced contractions as did the presence of the "Ca++ antagonists" verapamil (10- minus 5M), SKF 525-A (10- MINUS 5M), tetracaine (10- minus 4M), Mn++ (8 times 10- minus 3M), or La-3+ (10- minus 3M). In addition, it is no longer possible to produce tachyphylaxis to AII in deplorazed rat uterus under conditions of pH and Ca++ concentration in which a normally polarized preparation would be unresponsive. Verapamil, on the other hand, was an even more effective antagonist of AII in depolarized preparations (ID50 of 10- minus 8M) than in normal tissues (ID50 of 2.0 times 10- minus 7M). Like the rat uterus, the smooth muscle of the guinea pig ileum also develops tachyphylaxis to AII, and the effect of this peptide was also blocked by 10- minus 5 M verapamil. Rabbit aorta, however, was found to be relatively resistant to both development of tachyphylaxis under conditions of low Ca++ and low pH and also to inhibition by even very high concentrations of verapamil (10- minus 4M). The results of these studies suggest that the Ca++ site involved in the tachyphylactic response to AII may be a physiologically important one in those smooth muscles in which movement of extracellular Ca++ contributes to the inward ion currents during excitation. Verapamil, however, appears to act at a common step in the excitation-contraction sequence in rat uterus. A working model of the interaction of AII with rat uterine smooth muscle is presented.

Acetylcholine↗

PubMed1979

The role of sodium and potassium ions in the contractile response and development of tachyphylaxis to angiotensin II on vascular smooth muscle.

The role of sodium and potassium ions, and the possible involvement of the membrane sodium pump has been studied in the development of a contractile response to, and the development of tachyphylaxis to, angiotensin II. It is suggested that a membrane depolarization may have a role in the mechanism of the contractile response to angiotensin II, as responses of the rabbit aorta to angiotensin II were selectively inhibited in K-free medium. Acute or chronic increases in medium sodium, however, did not influence the response of the rabbit aorta to angiotensin II. On the rat aorta increased medium sodium concentrations potentiated the response to angiotensin II and inhibited the development of tachyphylaxis. Membrane depolarization or hyperpolarization does not appear to be part of the mechanism of development of tachyphylaxis to angiotensin II on the rat aorta, as response to both NE and angiotensin II were inhibited equally by exposure of the rat aorta to K-free medium, i.e., nonspecific desensitization occurred, as opposed to the specific desensitization which defines tachyphylaxis.

Angiotensin II↗

PubMed1976

The mechansim of tachyphylaxis to ICI 74,917 and disodium cromoglycate.

Pre-incubation in vitro of sensitised peritoneal mast cells for 10 min with either ICI 74,917 (10-5 M) abolished the ability of either drug to inhibit histamine release when subsequently presented to the cells at the same time as antigen. In the case of disodium cromoglycate, tachyphylaxis was abolished by washing the cells after pre-incubation with the drug. The failure to abolish tachyphylaxis to ICI 74,917 was due to the high pre-incubation concentration employed, as at lower concentrations (10-8 M) tachyphylaxis to ICI 74917 was readily abolished by washing. Tachyphylaxis to these anti-allergic agents may be related to a physical blocking of drug receptor sites on or in mast cells.

Animals↗

PubMed1979

Cross-tachyphylaxis of the pressor response to angiotensins in conscious rabbits.

The effect of tachyphylaxis to angiotensin II amide on the pressor potency of angiotensin I, II and III and noradrenaline was investigated in conscious rabbits with indwelling cannulae. No significant difference was observed between the reduction in responses to angiotensin II (58 +/- 4%) and angiotensin III (42 +/- 6%) but angiotensin I (15 +/- 5 %) and noradernaline (17 +/- 10%) responses were less markedly inhibited. If all angiotensin I pressor activity was mediated through its conversion to angiotensin II one would expect an equivalent degree of cross-tachyphylaxis to occur with the two peptides. Our results suggest that angiotensin I may have significant inherent pressor activity of its own, independent of conversion. This compound is already known to have activity at other target tissues. The absence of a significant difference in the degree of tachyphylaxis with angiotensin II and III may indicate they have substantially common pathways as pressor agents.

Angiotensin I↗

PubMed1977

Role of prostaglandins in the mediation of systemic tachyphylaxis to angiotensin II.

Angiotensin-induced prostaglandin release has been implicated in the deveolpment of tachyphylaxis to angiotensin in vitro. Based on these findings and evidence that prostaglandins modulate the angiotensin reposne locally, experiments were done to investigate the role of prostaglandins in the systemic tachyphylaxis to angiotensin. Rats were given intravenous infusions of 1-asparaginyl-5-valyl and 1-aspartyl-5-isoleucyl andiotensin II at two different doses. Using systemic blood pressure as a parameter, varying degrees of tachyphylaxis were produced and the aspartyl analog was found to be more tachyphylactic. When rats were given indomethacin, a prostaglading synthesis inhibitors, the response to intravenous infusion of aspartyl angiotensin was not significantly altered.

Angiotensin II↗