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PubMedDate not supplied

In vivo study of angiotensin II tachyphylaxis in freely moving normo- and hypertensive rats.

In vivo tachyphylaxis to the angiotensin II-induced increase in mean arterial blood pressure was studied in conscious freely moving rats by telemetry blood pressure monitoring. The animals studied were the normotensive Sprague Dawley rats (SD), the spontaneously hypertensive rats (SHR), and two models of experimentally-induced hypertensive rats, namely, the left renal artery stenosed SD hypertensive rat (LRAS) and the deoxycorticosterone acetate/salt SD hypertensive rat (DOCA). Two consecutive dose-response curves to angiotensin II in each rat were obtained. The increase in mean arterial pressure (MAP) at each bolus dose of the first dose-response curve was found not to be significantly different from the corresponding value of the second dose-response curve in the four models of rat studied (i.e. no significant difference in the intra-rat response to AII). In addition, the slope of the dose-response curve is similar for each model of rat indicating that there was no inter-model variation to the response of AII. The results show that the response to AII in the SD and the three models of hypertensive rats was remarkably similar and that they did not develop tachyphylaxis to the pressor response of AII at concentrations ranging from circulating level of 0.0005 nmoles/kg (10(-11) M) to 10 nmoles/kg (2 x 10(-7) M). This was despite the fact that the SD had normal blood pressure and the genesis of hypertension in each model of the hypertensive rats was different.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1975

The vascular changes after ephedrine tachyphylaxis.

The changes elicited after ephedrine tachyphylaxis in the dog femoral and rabbit aortic strips isolated from the untreated and ephedrine pre-treated animals have been studied. In untreated strips, ephedrine exhibited dose-dependent contractions which were blocked by phenoxybenzamine. These contractile responses to ephedrine were reduced after pre-treatment with ephedrine in vivo. In rabbit aortic strips previously contracted with noradrenaline or KCL, ephedrine induced dose-dependent relaxations at high concentrations, which were not affected by propranolol. These relaxation responses were likewise diminished after ephedrine. Dose-related contractile responses to noradrenaline were potentiated at low concentrations and depressed at high concentrations after ephedrine whereas those to adrenaline were inhibited over the entire agonist range. Responses to KCL were not affected. These reductions in the responses to noradrenaline and adrenaline after treatment with ephedrine in vivo were inhibited by icreased calcium2+ concentration. From the results, it can be presumed that the observed changes in vascular responsiveness may be partially involved in the development of ephedrine tachyphylaxis.

Animals↗
PubMed1975

Amphetamine tachyphylaxis in the pithed guinea-pig.

A single dose of (+)-amphetamine (8 mg kg-1, i.p.) administered 4 h before experimentation, reduced the pressor and positive chronotropic effects elicited by this drug (0-6 mg kg-1, i.v.) and augmented the rate of the development of tachyphylaxis to these responses in the pithed guinea-pig preparation. Amphetamine pretreatment reduced the pressor and positive chronotropic effects of phenylephrine (0-1 mg kg-1, i.v.) and the positive chronotropic effects of angiotensin (30 mug kg-1, i.v.). The rate of the development of tachyphylaxis to the cardiovascular responses elicited by phenylephrine and angiotensin was augmented by amphetamine pretreatment. The results suggest that an indirect mechanism (noradrenaline) may in part mediate the cardiovascular effects of these 3 drugs and/or that amphetamine may act as a competitive antagonist at adrenoceptor sites.

Angiotensin Amide↗
PubMed1961

Reversal of phenylalkylamine tachyphylaxis by norepinephrine.

Since the responses to "neurosympathomimetic amines" are reduced in the reserpinized animal and restored by norepinephrine administration, it was postulated that norepinephrine might also affect the development of their tachyphylaxis. We found that norepinephrine infusion restored, at least partially, certain tachyphylactic responses to amphetamine or ephedrine and fully prevented the development of tachyphylaxis to tyramine.

Amines↗
PubMed1984

Tachyphylaxis to PTH in the isolated perfused rat kidney: resistance of anticalciuria.

Downregulation of renal responses to amino-terminal 1-34 parathyroid hormone (PTH) was studied in the isolated perfused rat kidney. PTH induced a sigmoid dose-response relationship in phosphate and urinary cAMP excretion over the concentration range 0.2-36 nM. Renal responses to a second maximally phosphaturic PTH concentration following variable initial PTH concentrations showed tachyphylaxis of both phosphate and urinary cAMP excretion but not of decreased calcium excretion. The sigmoid relationship between integrated phosphate and cAMP excretion was shifted to the right during tachyphylaxis. Administration of a maximal phosphaturic PTH dose prevented any effect on phosphate or cAMP excretion of an equivalent or smaller PTH dose administered 1 h later. Anticalciuria, however, was prolonged by the second dose. These studies indicate that downregulation in the kidneys is restricted to the phosphaturic and urinary cAMP responses but not to the anticalciuric response. They also suggest that the nephron site mediating anticalciuria behaves differently with respect to hormone-receptor interactions from those sites mediating phosphaturia.

Animals↗
PubMed1985

Tachyphylaxis to inhaled aerosolized histamine in anesthetized dogs.

Three consecutive dose-response curves to inhaled aerosolized histamine, separated by 1-h intervals, were obtained in 20 anesthetized mongrel dogs. In general, successive histamine dose-response curves shifted progressively rightward. Changes in pulmonary resistance (RL) and dynamic compliance (Cdyn) in response to low concentrations of histamine were reproducible, but responses to high concentrations (sufficient to at least double RL or decrease Cdyn by at least 30%) decreased on successive dose-response curves. The concentration of histamine required to double RL increased significantly (P less than 0.05) from 1.01 mg/ml on the first to 1.62 and 2.02 mg/ml on the second and third dose-response curves. In contrast, consecutive methacholine dose-response curves were not significantly different. Indomethacin pretreatment (5 mg/kg iv) prevented histamine tachyphylaxis, whereas atropine (4 mg iv) did not. However, indomethacin did not alter base-line pulmonary mechanics or histamine responsiveness as measured on the first dose-response curve. We conclude that tachyphylaxis to inhaled aerosolized histamine occurs in anesthetized dogs. Our results are consistent with an important role for endogenous prostaglandins in modulating the airway responses to repeated histamine exposures.

Aerosols↗
PubMed1987

Hypocapnia-induced constriction of the canine peripheral airways exhibits tachyphylaxis.

Hypocapnia-induced constriction of peripheral airways may be important in regulating the distribution of ventilation in pathological conditions. We studied the response of the peripheral lung to hypocapnia in anesthetized, paralyzed, mechanically ventilated dogs using the wedged bronchoscope technique to measure resistance of the collateral system (Rcs). A 5-min hypocapnic challenge produced a 161 +/- 19% (mean +/- SE) increase in Rcs. The magnitude of this response was not diminished with repeated challenge or by atropine sulfate (1 mg base/kg iv), chlorpheniramine maleate (5 mg base/kg iv), or indomethacin (5 mg/kg iv). The response was reduced by 75% by isoproterenol (5 micrograms/kg iv) (P less than 0.01) and reduced by 80% by nifedipine (20 micrograms/kg iv) (P less than 0.05). During 30-min exposure to hypocapnia the maximum constrictor response occurred at 4-5 min, after which the response attenuated to approximately 50% of the maximum response (mean = 53%, range 34-69%). Further 30-min challenges with hypocapnia resulted in significantly decreased peak responses, the third response being 50% of the first (P less than 0.001). The inability of indomethacin or propranolol to affect the tachyphylaxis or attenuation of the response suggests that neither cyclooxygenase products nor beta-adrenergic activity was involved. Hence, hypocapnia caused a prompt and marked constrictor response in the peripheral lung not associated with cholinergic mechanisms or those involving histamine H1-receptors or prostaglandins. With prolonged exposure to hypocapnia there was gradual attentuation of the constrictor response with continued exposure and tachyphylaxis to repeated exposure both of which would tend to diminish any compensatory effect of hypocapnic airway constriction on the distribution of ventilation.

Airway Resistance↗
PubMed1996

Magnitude and determinants of short-term tachyphylaxis to methacholine in subjects with symptomatic or asymptomatic airway hyperresponsiveness and in normal controls.

Tachyphylaxis to methacholine has been reported in nonasthmatic subjects. In a recent study on the prevalence of airway hyperresponsiveness (AHR) and atopy, we performed duplicate methacholine inhalation tests at a 60-min interval, in subjects with symptomatic asthma (n = 33), asymptomatic AHR (AAHR) (n = 72) and in a group of normal subjects (n = 130); 135/235 subjects were atopic. All subjects had a respiratory questionnaire, allergy skin prick tests, blood eosinophil counts and determination of total serum IgE level. In asthmatic subjects, PC20 just failed to be significantly higher on a second methacholine challenge (p = 0.09); when they were stratified according to severity of AHR and use of inhaled corticosteroids, we observed a significant increase in PC20 on the second test in asthmatic subjects with mild AHR not using corticosteroids (p < 0.01). In normal controls, PC20 methacholine was slightly increased on rechallenge (p < 0.01) as it was in those with AAHR (p < 0.01). There was no relationship between the magnitude of the change in PC20 and age, sex, baseline airway responsiveness, percent fall in FEV1 on the first challenge, atopic score, blood eosinophil counts and serum IgE levels. In conclusion, tachyphylaxis to methacholine is observed in normal or mild asthmatic subjects not using inhaled corticosteroids and in subjects with AAHR; however, in most subjects this change is of a small magnitude.

Asthma↗
PubMed1989

Absence of tachyphylaxis to inhaled atropine in patients with chronic obstructive pulmonary disease.

A multicenter, 14-wk, double-blind, randomized, parallel group study of 60 patients with obstructive lung disease was performed to assess tachyphylaxis with inhaled atropine sulfate versus placebo. Forty patients completed the study; twenty-one were treated with placebo and nineteen were treated with atropine sulfate. Atropine and placebo groups were compared before and after inhaled atropine by spirometry at Weeks zero, 6, and 14. Medication side effects, other medication usage, and symptoms were recorded daily. Comparison of FEV1 response to atropine sulfate from baseline at Weeks zero, 6, and 14 did not show a statistically significant decrease. Inhaled atropine sulfate continued to be an effective bronchodilator in both placebo groups and atropine sulfate groups. There was no evidence of significant tachyphylaxis with atropine. Significant side effects in the atropine group when compared with placebo included dry mouth, dry skin, rapid heart rate, and nausea.

Administration, Inhalation↗
PubMed1990

Mechanism of tachyphylaxis associated with neurogenic plasma extravasation in the rat trachea.

Electrical stimulation of the vagus nerve of rats is known to produce plasma extravasation in the trachea, presumably by releasing substance P or other tachykinins from sensory nerves. We sought to determine whether the tachyphylaxis that develops after prolonged vagal stimulation results from an inability of sensory nerves to release tachykinins or from an inability of tracheal blood vessels to respond to tachykinins. To induce tachyphylaxis, we electrically stimulated the right vagus nerve of Long-Evans rats for 5 min (5 V, 1 ms, 20 Hz). Then, 10 min later, we gave intravenous injections of capsaicin (0.3 mumol/kg), histamine (18 mumols/kg), or substance P (2.2 nmol/kg), which produce equivalent amounts of plasma extravasation as assessed by the extravasation of Evans blue dye. We found that vagal stimulation reduced the amount of dye extravasation produced by capsaicin but not the amount produced by either histamine or substance P. We also found that pretreating neonatal rats with capsaicin, which destroys tachykinin-containing sensory nerves, reduced the amount of dye extravasation produced by capsaicin but not the amount produced by either histamine or substance P. This finding suggests that capsaicin produces plasma extravasation in the trachea by releasing tachykinins from sensory nerves, whereas histamine and substance P do so by acting directly on tracheal blood vessels. Taken together, our results indicate that prolonged vagal stimulation reduces the ability of sensory nerves to release tachykinins but that tracheal blood vessels remain fully responsive to both histamine and substance P.

Animals↗
PubMed2005

Lack of tachyphylaxis to methacholine at 24 h.

OBJECTIVE: To examine for tachyphylaxis to methacholine at 24 h and to use these data to assess the repeatability of the provocative concentration of a substance causing a 20% fall in FEV1 (PC20) for methacholine and to obtain statistical power calculations. DESIGN: Retrospective review of four double-blind, placebo-controlled studies with two methacholine PC20 values measured at 24-h intervals. SETTING: Tertiary university hospital bronchoprovocation laboratory. PATIENTS: Thirty-two subjects with mild-to-moderate well-controlled asthma. INTERVENTIONS: The placebo arms of the four studies were examined. MEASUREMENTS: Methacholine PC20 (using 2-min tidal breathing method) initial determination and repeat testing at 24 h. RESULTS: The geometric mean PC20 values were 1.57 mg/mL (95% confidence interval [CI], 1.0 to 2.4 mg/mL) and 1.62 mg/mL (95% CI, 1.0 to 2.6 mg/mL NSD; p = 0.64). The mean absolute difference between the two measurements was < 0.4 doubling concentrations, and 31 of 32 measurements had both values within one doubling concentration. These data provide a statistical power of 92% for 10 subjects to show a one-half concentration deltaPC20 and a mean power of 99 +/- 1% to show a one-concentration deltaPC20. CONCLUSIONS: There is no evidence for methacholine tachyphylaxis at 24 h in subjects with asthma. At 24 h, the average repeatability was well within a one-half concentration change, and individually 31 of 32 measurements (97%) were within one doubling concentration.

Adolescent↗
PubMed1988

Neurally mediated increase in vascular permeability in the rat trachea: onset, duration, and tachyphylaxis.

Electrical stimulation of the cervical vagus nerve of rats is known to increase vascular permeability in the trachea. In the present study, we sought to further characterize this neurogenic inflammatory response by defining the relationship between the parameters of electrical stimulation of the vagus nerve and the magnitude of the increase in vascular permeability, by determining the onset and the duration of the increase in vascular permeability, and by assessing the development of tachyphylaxis in response to consecutive periods of vagal stimulation. The extravasation of Evans blue dye in the trachea was used as an index of tracheal vascular permeability. Rats were injected intravenously with dye and their right vagus nerves were electrically stimulated. The rats were then prefused with fixative, their tracheas were removed, and the amount of extravasated dye in the tracheas was measured with a spectrophotometer. We found that a vagal stimulus of 5 V and 20 Hz for 15 s increased the amount of dye in the tracheas 5.5-fold compared to controls, that the dye extravasation began within 30 s of the start of vagal stimulation and lasted for 3-5 min, and that tachyphylaxis developed after a stimulus as brief as 15 s and reduced the dye extravasation produced by a subsequent period of vagal stimulation for up to 4 h.

Animals↗
PubMed1992

[The phenomenon of tachyphylaxis in the pathogenesis of an experimental infectious process].

Experiments on mice have revealed that the development of experimental purulent infection is accompanied by a considerable increase in the nonspecific resistance of the animals to additional infection with unrelated bacteria (the effect of tachyphylaxis). Morphologically, this is manifested by the rapid limitation of the focus of inflammation at the site of inoculation of the superinfecting agent. The state of the phagocytic apparatus is of great importance for this phenomenon as disturbances in the macrophage activity caused by the injection of carrageenan abolish the protective effect of primary infection. The phenomenon of tachyphylaxis has been shown to play a certain role in the prevention of the septic generalization of the process and in resistance to superinfection.

Animals↗
PubMed1990

Study of tachyphylaxis to the vasoconstrictor effect of arachidonic acid in the isolated perfused kidney of the rat.

The isolated perfused kidney of the rat was used to address the development of tachyphylaxis to the vasoconstrictor effects of arachidonic acid. Repeated administration of arachidonic acid (3 micrograms at 10-min intervals) to the isolated kidney of the rat, perfused in situ with Krebs-Henseleit solution, led to the development of tachyphylaxis to the renal vasoconstrictor effects of arachidonic acid, using perfusion pressure changes as an index. Vasoconstrictor responses to either angiotensin or the endoperoxide analog, U46619, were unaffected by repeated administration of arachidonic acid. Associated with progressively reduced renal vasoconstrictor responses to arachidonic acid were parallel decrements in the renal venous release of prostanoids, measured by radioimmunoassay. In contrast, the release of prostanoids from the kidney stimulated by angiotensin II was increased after repeated administrations of arachidonic acid. These data suggest that the sequential reduction in renal vasoconstrictor responses to arachidonic acid is due to diminished conversion to prostaglandins, possibly due to inactivation of cyclooxygenase, decreased entry of arachidonic acid into the cell or its increased esterification into phospholipids.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

[1-Sarcosine]-angiotensin II tachyphylaxis in helical strips and everted rings of rabbit aorta.

The development of tachyphylaxis to [1-sarcosine]-angiotensin II was studied in helical strips and everted rings of rabbit aorta. Strips, but not everted rings, developed marked (greater than 50%) tachyphylaxis to the peptide, when challenged repeatedly at 1-h intervals. Measurements of the membrane potentials showed no difference between the two preparations, but strips were more sensitive to KCl than everted rings. These results suggest that the strips are more depolarized than the everted rings due to lesions caused by the spiral cutting. This partial depolarization may underlie the tachyphylactic phenomenon.

Angiotensin II↗
PubMed1984

Venospastic activity of somatostatin in vivo in man: naloxone reversible tachyphylaxis.

When the dorsal hand vein (DHV) is locally injected with somatostatin (SS) it spasms visibly. These spasms can be measured using the computerized venospasm technique. Acute, complete long-lasting tolerance (tachyphylaxis) develops following 2-4 injections of somatostatin. A revival of sensitivity to SS is induced in the fatigued vein by the local injection of naloxone. This suggests that endogenous opioids could participate partially or totally in SS tachyphylaxis. The analgesic effect displayed by somatostatin on the dramatic pain of the cluster attack is quantitatively similar to that of ergotamine; the therapeutic mechanism of both drugs has until now remained undefined.

Adult↗
PubMed1982

Plasma cholinesterase activity and tachyphylaxis during prolonged succinylcholine infusion.

Fifteen patients were studied during general anesthesia (nitrous oxide-fentanyl, N = 7 or nitrous oxide-isoflurane, N = 8) to determine the relationship between plasma cholinesterase activity and succinylcholine requirements during prolonged infusion. Using train-of-four stimulation, neuromuscular block was maintained at 90% for at least 1 hour, and plasma cholinesterase was measured at 30-minute intervals. During the infusion, succinylcholine requirements increased in every patient (tachyphylaxis), but there was no significant change in plasma cholinesterase activity. Succinylcholine requirements during the 1st hour of infusion in patients given fentanyl were correlated with preinfusion cholinesterase activity. It is concluded that tachyphylaxis to succinylcholine is not the result of increased metabolism from enzyme induction and that succinylcholine requirement is related to plasma cholinesterase activity.

Cholinesterases↗
PubMed1996

Different classes of PAF-antagonists block norepinephrine-induced vascular escape and tachyphylaxis in the isolated rabbit kidney.

In order to study the role of platelet activating factor (PAF) on norepinephrine induced vascular escape and tachyphylaxis, compounds from different pharmacological families sharing PAF-antagonistic activity, were infused in the isolated rabbit kidney perfused with Krebs-Henseleit solution. A natural compound derived from Ginkgo biloba (BN 52020, 1.1 x 10(-6) M), a triazolobenzodiazepine substance (WEB 2170, 1.1 x 10(-6) M) and a dihydropyridine derivative lacking cardiovascular effects (PCA 4248, 2.7 x 10(-6) M), were analysed. The vascular reactivity to three cycles of norepinephrine (1.3 x 10(-6) M), infused in the kidneys treated with each of the PAF- antagonists, were evaluated for vascular escape and tachyphylaxis. The results demonstrated a significant reduction of both regulatory phenomena. A fall in renal vascular escape promoted by PAF antagonists, from a control level of 50.32 +/- 4.61 to 27.64 +/- 8.01% (p < 0.05), suggests a role for PAF-acether in the vascular adjustment of the mammalian kidney.

Animals↗