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PubMed1982

Renal vascular tachyphylaxis to angiotensin II: specificity of the response for angiotensin.

Hypotheses concerning angiotensin's role in states characterized by severe and sustained renal vasoconstriction, must account for the poorly sustained renal response to this agent in healthy animals and man. To assess the specificity of renal vascular tachyphylaxis to angiotensin II (AII), renal blood flow was measured with an electromagnetic flowmeter in eight anesthetized dogs. Bolus injections of AII and norepinephrine into the renal artery were adjusted to produce at least a 50% reduction in renal blood flow, and were followed by a continuous infusion of AII sufficient to reduce renal blood flow acutely by 60 +/- 10%. The response to the continuous infusion was poorly sustained, blood flow returning to near baseline within 10 minutes: At this time the response to bolus administration of AII was lost, but the response to norepinephrine was sustained. At 30 minutes the response to norepinephrine was also reduced, and there was no response in three of the eight dogs. After stopping the AII infusion, renal vascular responsiveness to norepinephrine returned almost immediately, but 30-60 minutes were required before responsiveness to AII was restored. We conclude that there is true, specific renal vascular tachyphylaxis to AII--which may well reflect receptor modulation or occupation--and that with time an additional, non-specific vasodilator mechanism can come into play.

Angiotensin II↗
PubMed1993

Characteristics and mechanisms of tachyphylaxis of cardiac contractile response to insulin.

Although insulin is known to cause internalization of its own receptors, the physiological significance of this phenomenon is not clear. In the isolated rat heart we observed that the positive inotropic effect of 25 munits/ml insulin was completely abolished if the heart was preperfused with insulin for 10 min. This tachyphylactic response to insulin began to appear 3-4 min after starting preperfusion with insulin and was partially reversible after 30 min of washing. Preperfusion with insulin did not affect the action of vanadate, which has insulin-like effect on glucose transport, or the actions of the other positive inotropic agents, isoproterenol and ouabain. The presence of propranolol in the perfusion medium, unlike atenolol, phenoxybenzamine, guanethidine, verapamil or quinidine, modified the inotropic as well as tachyphylactic responses to insulin. The positive inotropic and tachyphylactic responses to insulin were not altered in hearts from reserpine-treated animals. Perfusion of heart with glucose-free solution abolished the tachyphylaxis due to insulin. Likewise, no tachyphylactic response to insulin was evident when iodoacetate, but not sodium fluoride, was added in medium containing glucose. These results suggest that ATP formed during glycolysis may play an important role in insulin-induced tachyphylaxis with respect to cardiac contractile activity.

Adenosine Triphosphate↗
PubMed1984

Antidepressant tachyphylaxis.

We report eleven patients in whom tachyphylaxis to antidepressants, lithium or ECT occurred. These cases are a small sample of patients we have encountered in whom an initial good response to mood regulating drugs was not sustained. We suspect that systematic studies would reveal that tachyphylaxis is a common phenomenon with antidepressant therapies.

Adult↗
PubMed1998

Caliber dependent calcitonin gene-related peptide-induced relaxation in rat coronary arteries: effect of K+ on the tachyphylaxis.

The influence of vessel caliber on rat calcitonin gene-related peptide (rat-alphaCGRP)-induced responses and the reproducibility of rat-alphaCGRP concentration-response curves were investigated in the left intramural coronary artery of Sprague-Dawley rats. Rat-alphaCGRP (10(-11)-10(-7) M) induced concentration-dependent relaxations with a pD2-value equal to 8.43 +/- 0.05 (n = 44) and maximal relaxation equal to 52 +/- 3% (n = 44). Both the maximal relaxation and the sensitivity to rat-alphaCGRP were significantly and inversely correlated with vessel lumen diameter. The coronary arteries developed tachyphylaxis in response to rat-alphaCGRP, which was concentration dependently decreased by activating the vessels twice with a buffer containing 36 or 125 mM K+. The rat-alphaCGRP-curve became fully reproducible after activation of the arteries twice with 125 mM K+. These results indicate a caliber-related dependency of both the effect of and sensitivity to rat-alphaCGRP in intramural rat coronary arteries because the arteries become more sensitive and reactive to rat-alphaCGRP with decreasing caliber. Tachyphylaxis can be avoided by repeated activation with 125 mM K+.

Animals↗
PubMed1990

Tachyphylaxis to inhaled histamine in asthma: its significance and relationship to basal airway responsiveness.

Although some studies have clearly demonstrated tachyphylaxis to inhaled histamine in subjects with asthma, other studies have not. We speculated that histamine tachyphylaxis might be related to the degree of bronchial hyperreactivity (BHR) to histamine. We undertook three successive bronchial histamine challenges in two groups of 10 subjects with asthma chosen on the basis of their baseline BHR. In the group with mild asthma, the baseline provocative concentration of histamine causing a 20% fall in FEV1 (PC20) was greater than 2.5 mg/ml, and in the group with severe asthma, the baseline PC20 histamine was less than 1 mg/ml. The second and third histamine challenges in each subject were performed when FEV1 values had recovered to within 5% of the baseline FEV1 before the first challenge. There was no significant shift in reactivity to histamine from the first to the third challenge in either group. The geometric mean PC20 (+/- geometric SE) for the group with mild asthma was 4.27 (3.86 to 4.72) mg/ml for the first challenge and 5.42 (4.47 to 6.57) mg/ml for the third challenge. There was a mean increase of 0.34 doubling dilutions in PC20 for the group with mild asthma from the first to the third challenge, although this did not reach statistical significance. For the group with severe asthma, the geometric mean PC20 was 0.48 (0.39 to 0.59) mg/ml for the first challenge and 0.47 (0.38 to 0.59) mg/ml for the third challenge. There was no trend in this group toward any increase in PC20.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Acute tachyphylaxis to propofol sedation during ethanol withdrawal.

We treated a patient with a 30-year history of ethanol and benzodiazepine abuse who, on emerging from general anesthesia, was combative and confused. Our working diagnosis was acute ethanol withdrawal, and the patient received intravenous (i.v.) propofol, and midazolam. Initially small doses (10 to 20 mg) of propofol, combined with a midazolam infusion (50 mg/hr), produced sedation. Later, however, the patient became increasingly combative, confused, hypertensive, and tachycardic despite an i.v. propofol infusion at doses up to 1,000 micrograms/kg/min (total propofol dose: 1,755 mg). Immediate sedation was produced by thiopental bolus (500 mg) and i.v. infusion (200 mg/hr). The implication of the patient's initial appropriate response to propofol, followed by the lack of effect when much higher doses were employed, is discussed. While tachyphylaxis has been reported after long-term propofol use, we believe this to be the first case of acute tachyphylaxis.

Acute Disease↗
PubMed1988

Influence of topical phenylpropanolamine on tachyphylaxis and mucociliary clearance in the human nose.

Topical nasal phenylpropanolamine in a 2.5 per cent solution (PPA) was used in an evaluation of the possible development of tachyphylaxis and of possible effects on the mucociliary system after one week of treatment in healthy humans. The tendency of PPA to produce tachyphylaxis was evaluated by rhinomanometrie measurements of nasal airway resistance after repeated dose-response provocations. The mucociliary transport time was tested with the saccharine-dye test. No reduced dose-response effect or change in mucociliary transport time was found with PPA, thus indicating that one week of treatment does not contribute to such adverse effects.

Adolescent↗
PubMed1983

Impaired 5-hydroxytryptamine tachyphylaxis in migraine.

Tachyphylaxis (TPX) to the spasmogenic activity of 5HT can be demonstrated in vivo in the superficial hand dorsal veins in man by the computerized venotest. The 5HT-TPX is reverted by previous local naloxone administration. Tachyphylaxis to 5HT is usually absent in the migraineur. The restored 5HT spasmogenic effect by naloxone suggests the possibility of local opioid apparatus participation in TPX to 5HT.

Adolescent↗
PubMed1980

[Tachyphylaxis in timolol therapy for chronic glaucoma (author's transl)].

Forty-three patients with open-angle glaucoma were treated locally with 0.5% Timolol. The drop in intraocular pressure on the day following commencement of Timolol therapy was remarkable. However, 14 patients, ten of whom had responded insufficiently to other glaucoma drugs, developed tachyphylaxis either two or three days after being put on Timolol therapy; in some cases tachyphylaxis was observed in follow-up examinations two months later. Intraocular pressure in these eyes was in some cases even higher than it had been prior to treatment with Timolol.

Adolescent↗
PubMed1975

Dose relationships of phase II, tachyphylaxis and train-of-four fade in suxamethonium-induced dual neuromuscular block in man.

In man under halothane-nitrous oxide-oxygen anaesthesia, suxamethonium-induced neuromuscular block can be divided into two phases using the train-of-four ratio: the first phase of minimal train-of-four fade and the second phase of marked train-of-four fade. The second phase is characterized by a low train-of-four ratio, 0.3 or less, and resembles tubocurarine-block) in many details. It corresponds to Phase II (dual block in the literature. Contrary to the prevailing belief, Phase II block has a rather abrupt onset. In this study of seven patients, Phase I covered up to a total of 1--3 mg/kg of suxamethonium, while 3--5 mg/kg established Phase II block, with a transitional zone of only 2 mg/kg. Establishment of Phase II also coincided with onset of unequivocal tachyphylaxis. The possibility of a causal relationship between tachyphylaxis and Phase II block is suggested.

Adult↗
PubMed2003

Up and down-regulation of phosphodiesterase-5 as related to tachyphylaxis and priapism.

PURPOSE: We identify whether tachyphylaxis and priapism effects of sildenafil are related to regulation of phosphodiesterase-5 (PDE-5) expression. MATERIALS AND METHODS: Cavernous smooth muscle cells (CSMCs) were isolated from young rats and treated with 0, 1, 10 and 25 microM sildenafil with or without 100 microM of sodium nitroprusside for 3 and 7 days. The cells were subjected to reverse transcriptase-polymerase chain reaction and Western blot analysis for PDE-5 expression. Plasmid constructs carrying PDE-5A1 and PDE-5A2 promoters were transfected into COS-7 cells, treated with 25 microM sildenafil and analyzed for promoter activities. To simulate priapism, CSMCs were cultured under anoxia or hypoxia and then analyzed for PDE-5 expression. Furthermore, rats underwent bilateral pudendal arterial ligation for 1 day to 14 weeks, and corpus cavernous tissues were subjected to reverse transcriptase-polymerase chain reaction analysis for PDE-5 expression. RESULTS: Up-regulation of PDE-5 was noted in CSMCs treated with 25 microM sildenafil for 7 days. PDE-5 messenger RNA and protein levels were significantly increased in the 7-day sildenafil treated cultures. Sodium nitroprusside appeared to down-regulate PDE-5 expression. Sildenafil significantly increased the activities of PDE-5A1 promoter. PDE-5 expression was significantly reduced under anoxia and hypoxia. The corpus cavernous tissue showed a gradual decrease in PDE-5 expression under ischemia. CONCLUSIONS: Repeated treatment with sildenafil at high concentrations was needed to simulate tachyphylaxis in our cell culture system. Adequate oxygenation was important for PDE-5 expression. Thus, sicklemic patients may express PDE-5 at abnormally low levels, predisposing them at risk of stuttering priapism.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1980

Tachyphylaxis to beta-adrenoceptor agonists in human bronchial smooth muscle: studies in vitro.

In studies on human isolated peripheral airway smooth muscle; 1 A concentration dependent beta-adrenoceptor tachyphylaxis was observed to isoprenaline. 2 Cross desensitization to other beta-adrenoceptor agonists was demonstrated. 3 The desensitization was reversible with time. Hydrocortisone appeared to accelerate the recovery from the desensitized state. Low concentration isoprenaline (10(-9) mol l-1) prevented recovery whereas cyclohexamide 1.8 x 10(-4) mol l-1 had no noticeable effect on recovery. Continued occupancy of the receptor appears to prevent recovery. The recovery from the desensitized state does not apparently require synthesis of new proteins. 4 Bronchial wall cyclic AMP response to isoprenaline was attenuated after isoprenaline induced desensitization whereas total phosphodiesterase activity of bronchial wall was not altered by desensitization. Thus by exclusion the adenylate cyclase receptor complex may be altered in human peripheral airway smooth muscle beta-adrenoceptor tachyphylaxis.

Adrenergic beta-Agonists↗
PubMed1994

Does tachyphylaxis occur to the non-pulmonary effects of salmeterol?

1. The potential for tachyphylaxis to the non-pulmonary effects of salmeterol, a long-acting selective beta 2-adrenoceptor agonist was investigated in 12 healthy male subjects in a double-blind two period crossover study design. 2. Subjects received cumulative doses of up to 400 micrograms (50 + 50 + 100 + 100 + 100 micrograms at 45 min intervals) inhaled salmeterol prior to a 13 day dosing schedule of twice-daily inhaled salmeterol 100 micrograms or placebo. Twelve hours after the last dose of salmeterol or placebo, subjects again received cumulative doses of up to 400 micrograms inhaled salmeterol. 3. Pulse rate, blood pressure, 12-lead ECG, physiological tremor and peak expiratory flow rate (PEFR) were measured before administration of cumulative doses of salmeterol, at 10, 20, 30 and 40 min after each incremental dose of salmeterol and at 4, 6 and 8 h after the first dose. Blood samples were taken for plasma potassium, magnesium, non-esterified fatty acids (NEFA) and blood glucose concentrations at 20 and 40 min after each dose and at 4, 6 and 8 h after the first dose. 4. Eleven subjects completed the study. One subject withdrew due to beta 2-adrenoceptor related adverse events. All other adverse events reported were mild in nature. 5. Dose-related changes to the effects of salmeterol on pulse rate, QTc interval, tremor, PEFR, blood glucose and plasma potassium were seen, but there was no dose-related effect of salmeterol on blood pressure, plasma magnesium and NEFA. 6. Tachyphylaxis occurred to the effects of salmeterol on tremor, QTc and blood glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1986

Tachyphylaxis to topical steroid measured by histamine-induced wheal suppression.

Ten healthy volunteers were studied to find out whether tachyphylaxis occurs on repeated application of topical steroids. The Singh and Singh modification of the Reddy and Singh (1976) technique was used. Fluocinolone acetonide cream (0.1%) under occlusion was applied daily for 14 days on the flexor aspect of the forearms. The wheal was induced by pricking with histamine acid phosphate solution and the volume of the wheal produced was calculated. The test was repeated on the same sites on alternate days for 14 days. The maximum wheal suppression, which gradually diminished, was observed on the 8th day. By the 14th day, there was practically total tolerance to topical steroid, which showed minimal suppression of histamine wheal formation. This confirms the occurrence of the phenomenon of tachyphylaxis by different experimental techniques.

Administration, Topical↗
PubMed2006

Evidence of tachyphylaxis associated with salmeterol treatment of chronic obstructive pulmonary disease patients.

Bronchodilator therapy is lifelong mandatory for chronic obstructive pulmonary disease patients. There is evidence of loss of bronchodilator effectiveness over time with beta2-agonists but not with anticholinergics. The aim of this study was to examine the development of tachyphylaxis to the long-acting beta2-agonist salmeterol using as a control therapeutic regimen the combination of ipratropium bromide and salbutamol sulphate. Fifty-six subjects participated in a 20-week, crossover randomised clinical trial. The parameters forced expiratory volume at 1 s (FEV1), peak expiratory flow rate (PEFR) and FEV1/forced vital capacity were measured via spirometry and the parameters triangle DeltaFEV1%pre, triangle DeltaPEFR%pre and triangle DeltaAUC(0-2 h) were calculated. FEV1 increased significantly after two weeks of treatment with the combination treatment but not with the salmeterol. The observed diminished increase could be attributed to the development of tolerance to the long acting beta2-agonist. Salmeterol seems to be an effective bronchodilator, however, its duration of action over time and its peak effect might be subject to tachyphylaxis.

Adrenergic beta-Agonists↗
PubMed1977

The effects of intraportal injections of noradrenaline, adrenaline, vasopressin and angiotensin on the hepatic portal vascular bed of the dog: marked tachyphylaxis to angiotensin.

1 The hepatic portal vein of the anesthetized dog was cannulated and perfused with blood derived from the cannulated superior mesenteric vein. 2 The portal vein was perfused at constant flow, the hepatic portal venous pressure being monitored continuously together with the inferior vena caval pressure. From these measurements, the hepatic portal venous vascular resistance was calculated. 3 Noradrenaline and adrenaline were injected intraportally in graded doses which caused dose-dependent increases in the hepatic portal vascular resistance. At all doses, adrenaline was significantly (P less than 0.05) more potent than noradrenaline. 4 Intraportal injections of vasopressin caused reductions in calculated hepatic portal venous vascular resistance in most experiments; three effects were dose-dependent. 5 No tachyphylaxis to the effects of noradrenaline, adrenaline or vasopressin was observed. 6 Intraportal injections of angiotensin caused dose-dependent increases in calculated hepatic portal vascular resistance up to 5 mug; therafter larger doses caused smaller increases in portal resistance. 7. Repeated intraportal injections of angiotensin revealed the existence of tachyphylaxis in the hapatic portal vascular bed. 8 Intraportal infusions of anagiotensin caused rises in calculated hepatic portal vascular resistance from which there was almost complete 'escape' despite the continued infusions. Infusions of noradrenaline which caused similar rises in calculated portal vascular resistance did not exhibit equivalent degrees of 'escape'. 9 The development of tachyphylaxisx explains the fact that doses of 10 and 20 mug of angiotensin injected after 5 mug doses produced smaller effects. If a much longer time interval was allowed between injections (30 min), the dose-response curve to angiotensin had a sigmoid shape. 10 These findings are discussed with respect to their possible importance in the functional status of the hepatic portal vascular bed in this species.

Angiotensin II↗
PubMed1978

Tachyphylaxis to ethacrynic acid in the isolated atrium of guinea-pig and its relation to noradrenaline stores.

1 The isolated electrically-paced atrium of the guinea-pig developed a dose-dependent increase in the force of contraction in response to ethacrynic acid (12-100 microgram/ml) which was blocked by pretreatment of the animals with reserpine but was unaffected by desipramine or colchicine added to the bathing medium. 2 There was a rapidly developing tachyphylaxis to repeated doses of ethacrynic acid which was not reversed by rest or incubation of the tissue with noradrenaline. 3 There was no cross tachyphylaxis between ethacrynic acid and tyramine, amphetamine or nicotine. 4 Ethacrynic acid (200 microgram/ml) decreased the noradrenaline content of the atria by 32%. 5 It is concluded that ethacrynic acid exerts its effects indirectly through the release of endogenous noradrenaline and that the mechanism of release seems to be different from that of other known indirect sympathomimetic drugs.

Animals↗
PubMed1991

TRH-induced tachyphylaxis: present in the smooth muscle but not in the cardiorespiratory effects.

The development of tachyphylaxis to the pressor, tachycardiac, ventilatory and smooth muscle effects of thyrotropin-releasing hormone (TRH) was studied. Subsequent administrations of increasing doses of TRH (0.1-1000 nmol/kg intracerebroventricularly), at 20 min. intervals in urethane-anesthetized rats dose-dependently increased the mean arterial blood pressure, heart rate and minute ventilation volume. At all doses the effect on mean arterial blood pressure was apparent at least 20 min. after each injection whereas at low doses (0.1-1 nmol/kg) the duration of the effects on heart rate or minute ventilation volume were shorter. The cardiorespiratory effects of TRH 10 nmol/kg intracerebroventricularly did not subside completely within an observation period of 1 hr. However, a repeated administration of TRH at 1 hr resulted in the levels of mean arterial blood pressure, heart rate and minute ventilation volume not statistically different from the peak levels of the first injection. While the cardiorespiratory effects of TRH were long-lasting, the TRH induced inhibition of the contractions of the rat duodenal smooth muscle lasted only 12-18 sec. The TRH-treated duodenal preparation responded normally to noradrenaline but remained unresponsive to further administrations of TRH until washed extensively. When the medium after cessation of the TRH response was transferred into another chamber with an untreated preparation, a full response was resulted. Inhibitors of TRH metabolism, bacitracin, EDTA and iodoacetamide, did not prolong nor enhance the response. Likewise, a stable TRH-analogue MK-771 did not produce any longer response than TRH. It is concluded that no tachyphylaxis was produced to the neurally mediated pressor, tachycardiac or ventilatory effects of TRH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗