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PubMed1986

Actions of cardiotoxins from the southern Chinese cobra (Naja naja atra) on rat cardiac tissue.

The cardiotoxic actions of southern Chinese cobra (Naja naja atra) venom have been investigated. Cardiotoxicity accounted for lethality of crude venom in anaesthetized rats and cardiotoxic polypeptides constituted the bulk of the venom when it was fractionated by CM-Sephadex chromatography. The cardiotoxic actions of these polypeptides were investigated in isolated cardiac tissue. Actions of cardiotoxins on rate, force and intracellular potentials occurred more readily in ventricular tissue and were reversible in all cardiac tissues. Bolus injections of cardiotoxins to perfused rat hearts produced profound changes in intracellular potentials, but such changes were reversed by 10 min after toxin wash-out. The changes included depolarization and loss of the fast phase (0) of the action potential. The loss of beating and contracture produced by cardiotoxins in isolated atria and ventricles showed such marked tachyphylaxis that toxicity was lost after 2-5 exposures. Both calcium and heparin ameliorated the cardiotoxic actions of cardiotoxins. Since the actions of cardiotoxin were partially selective for ventricular tissue, reversible, demonstrated tachyphylaxis and could be prevented, it is suggested that a specific molecular mechanism may be involved, rather than a non-specific action such as cell membrane destruction.

Animals↗
PubMed1993

Mechanisms of the secretory response to luminal propionate in rat descending colon in vitro.

Short chain fatty acids stimulate Cl secretion in rat descending colon in vitro via an enteric reflex involving mucosa and cholinergic nerves. We used the short circuit current as the measure of Cl secretion caused by Na propionate (NaP) (0.5 mM) in luminal bath fluid and studied the mechanism of the response. The NaP response was decreased 81% by atropine and 76% by lidocaine. It was unaffected by tetrodotoxin, omega-conotoxin or by tachyphylaxis to capsaicin, CGRP, substance P, histamine or PGE2. It was not reduced by inhibitors of 5-HT2 or 5HT3 receptors or by partial tachyphylaxis to 5-HT. However, superficial mucosal injury with hypertonic Na sulfate (2 M) or xylose (4.5 M) reduced the NaP response by 90% and 86%, respectively, and mucosal concanavalin A (1 mg/ml) reduced it by 73%. Neither piroxicam (10 microM) nor nordihydroguaretic acid (10 microM) affected the NaP response. We hypothesize that NaP stimulates the superficial epithelium to release an unidentified agonist that depolarizes predominantly cholinergic nerve terminals and causes colonic secretion.

Acetylcholine↗
PubMed1987

Somatostatin: peripheral venoconstrictive activity and interaction with monoamines in man.

The mechanism of somatostatin venoconstriction and tachyphylaxis in the human hand vein in vivo has been investigated. No cross-tachyphylaxis was observed between somatostatin and 5-hydroxytryptamine, noradrenaline, adrenaline, dopamine or tyramine-induced venoconstriction. Somatostatin potentiates the venoconstrictive activity of noradrenaline, adrenaline and dopamine, but not that of 5-hydroxytryptamine and tyramine. Phentolamine antagonizes the somatostatin-induced venoconstriction, whereas methysergide, haloperidol and morphine do not. It is suggested that somatostatin could act on specific receptors in the hand vein, but the mechanism of somatostatin venoconstriction and interaction with vasoactive monoamines remains to be defined.

Adult↗
PubMed1987

The effects of arginine-8 vasopressin on blood vessels supplying the cerebral cortex.

A videocamera and a dissecting microscope have been used to record the effects of arginine-8 vasopressin (AVP) upon pial blood vessels in anaesthetised rats. Topical application of AVP caused a contraction of pial arteries, but had no measureable effect upon the diameter of veins. The smallest concentration of AVP that was effective in contracting arteries was 10(-7) mU/microliter. Stronger solutions (10(-5) to 2.0 mU/microliter) produced approximately the same (45%) reduction of external diameter. Contraction was maximal 0.25-1.0 min after application of the hormone, had almost recovered (10% contraction) after 10 min, and showed complete recovery by 30 min. Concentrations of AVP that were greater than 10(-3) mU/microliter produced tachyphylaxis, so that a second application of AVP 30 min later had considerably less effect. Concentrations less than 10(-3) mU/microliter produced no detectable tachyphylaxis. These results suggest that blood flow to the normal cerebral cortex may be partly under tonic control by the local concentration of AVP.

Animals↗
PubMed1983

C5a and antigen-induced tracheal contraction: effect of a combination of an antihistamine and cyclo-oxygenase inhibitors.

Our previous studies with C5a, a cleavage product of the fifth component of complement, have shown that the antihistamine diphenhydramine and the cyclo-oxygenase inhibitor aspirin do not inhibit the C5a-induced contraction of isolated guinea pig trachea (Regal, Eastman & Pickering, 1980; Regal & Pickering, 1981). We investigated the effect of cyclo-oxygenase inhibitors in the presence of diphenhydramine to determine if cyclo-oxygenase products were contributing to the contraction beyond any effect they might have on histamine release. A combination of a cyclo-oxygenase inhibitor and diphenhydramine caused a delay in onset and decrease in magnitude and duration of the C5a-induced contraction. Indomethacin itself also caused a slight inhibition. In contrast, a combination of aspirin and diphenhydramine did not inhibit the initial portion of antigen-induced tracheal contraction any more than diphenhydramine alone and enhanced the later portion just as aspirin alone. Cross tachyphylaxis experiments demonstrated that antigen pretreatment significantly inhibited a subsequent C5a-induced tracheal contraction, though C5a pretreatment did not affect a subsequent antigen-induced contraction. Thus, cyclo-oxygenase products do contribute to C5a-induced tracheal contraction, and histamine participation in the presence of cyclo-oxygenase inhibitors is suggested. Our studies demonstrate the dissimilarities of C5a and antigen-induced contraction as regards inhibition by aspirin plus diphenhydramine, yet suggest common pathways leading to the contractile response as evidenced by cross tachyphylaxis experiments.

Animals↗
PubMed2004

The effect of daily use of brimonidine tartrate on the dark-adapted pupil diameter.

PURPOSE: To investigate the effect of daily brimonidine tartrate 0.15% on the dark-adapted pupil diameter. DESIGN: Observational case series. METHOD: Ten normal volunteers administered brimonidine to their right eyes once daily. Four to six hours later, infrared pupil photographs were taken after dark adaptation. Measurements were performed at baseline; on treatment days 1, 5, 11, and 18; and on washout days 1 and 2. RESULTS: One subject had no response. The nine responding subjects showed an average maximum antimydriatic effect of -1.63 mm (range, -0.57 mm--2.30 mm); all subjects experienced tachyphylaxis. Five subjects showed rebound mydriasis (mean maximum rebound +0.87 mm larger than baseline; range 0.50 mm-1.22 mm). The untreated pupil also responded, showing antimydriasis (two subjects), rebound mydriasis (two subjects), or paradoxical direct mydriasis (one subject). CONCLUSIONS: Once-daily use of brimonidine tartrate to prevent dark-induced pupil dilation can lead to tachyphylaxis and rebound mydriasis.

Adolescent↗
PubMed2004

Activation of protein kinase C reverses capsaicin-induced calcium-dependent desensitization of TRPV1 ion channels.

Ca2+ selective ion channels of vanilloid receptor subtype-1 (TRPV1) in capsaicin-sensitive dorsal root ganglion (DRG) neurons and TRPV1 transfected Chinese hamster ovarian (CHO) cells are desensitized following calcium-dependent tachyphylaxis induced by successive applications of 100 nM capsaicin. Tachyphylaxis of TRPV1 to 100 nM capsaicin stimuli was not observed in the absence of extracellular calcium. Capsaicin sensitivity of desensitized TRPV1 ion channels recovered on application of phorbol-12-myristate-13-acetate (PMA). PMA-induced recovery of desensitized TRPV1 was primarily due to influx of extracellular calcium observed during re-application of capsaicin following desensitization. Capsazepine blocked the re-sensitization to capsaicin by PMA. Protein kinase C (PKC) inhibitory peptide PKC fragment 19-36 also inhibited re-sensitization to capsaicin by PMA. Reversal of capsaicin-induced desensitization by PMA was prevented by a mutation of TRPV1 where phosphorylation sites serine502 and serine800 were replaced with alanine. This study provides evidence for a role of PKC in reversing capsaicin-induced calcium-dependent desensitization of TRPV1 ion channels.

Amino Acid Substitution↗
PubMed1996

Contraction inhibition by beta-agonists progressively decreases before labor in the rat myometrium.

OBJECTIVE: This study tested the hypothesis that gestational age and agonist concentration are important determinants of beta-adrenergic-dependent myometrial contraction inhibition. STUDY DESIGN: In vitro concentration-response curves for ritodrine and terbutaline were generated with myometrial strips collected from 21-day-pregnant rats. The in vitro efficacy of ritodrine (0.1 mumol/L) was evaluated in tissue from 15-, 18-, and 21-day animals. Contractile responses were analyzed by computer and normalized to a control potassium response. RESULTS: The degree of the inhibitory effects of both drugs was concentration dependent over the range of 0.01 to 10 mumol/L. The duration of contraction inhibition progressively decreased from 15 to 21 days of pregnancy. CONCLUSION: The degree of tachyphylaxis with beta-agonists is dependent on and increases with the gestational age of the target tissue. beta-Agonist type was not an important determinant of the duration of inhibitory response. We speculate that the effect of gestational age on tachyphylaxis may be related to increased myometrial expression of inactivating beta-adrenergic receptor kinases.

Adrenergic beta-Agonists↗
PubMed2003

Angiotensin II-mediated cellular responses: a role for the 3'-untranslated region of the angiotensin AT1 receptor.

We have previously demonstrated that Chinese hamster ovary (CHO) cells transfected with the angiotensin II AT1 receptor gene containing only the coding region, presented tachyphylaxis to the total inositol phosphate (InsPs) and Ca2+ responses mediated by angiotensin II and [2-lysine]angiotensin II ([Lys2]angiotensin II). Now we have evaluated the possible role of the 3'-untranslated region of the angiotensin AT1 receptor mRNA in modulating the angiotensin AT1 receptor-mediated cellular responses. The binding parameters, as well as the Ca2+ and InsPs responses induced by angiotensin II and [Lys2]angiotensin II were similar in cells transfected with the angiotensin AT1 receptor with or without the 3'-untranslated region sequence. In cells transfected with the receptor containing the 3'-untranslated region sequence, angiotensin II-induced Ca2+ and InsPs responses were desensitized by repeated stimulations, whereas [Lys2]angiotensin II caused desensitization of InsPs production but not of Ca2+ uptake in these cells. Our results suggest that the 3'-untranslated region plays a role in modulating cell signalling involved in the tachyphylaxis of angiotensin AT1 receptor-mediated Ca2+ responses.

3' Untranslated Regions↗
PubMed1997

Heterologous desensitization of beta-adrenoceptor signal transduction in vivo.

The hemodynamic actions of pituitary adenylate cyclase-activating polypeptide (PACAP-27) rapidly diminish upon repeated i.v. injection in rats treated with the nitric oxide synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME). We now report that the beta-adrenoceptor agonist isoproterenol (0.5 microg/kg, i.v.) produces pronounced hypotensive and vasodilator effects in anesthetized rats pretreated with L-NAME (100 micromol/kg, i.v.). However, the hypotensive and vasodilator actions of isoproterenol were markedly diminished in L-NAME-treated rats in which tachyphylaxis to PACAP was induced immediately prior to the injection of the beta-adrenoceptor agonist. This suggests that a reduction in tissue concentrations of nitric oxide-containing factors allows tachyphylaxis to PACAP-27-mediated vasodilation to occur in vivo and that this process leads to the heterologous desensitization of beta-adrenoceptor-mediated responses.

Adrenergic beta-Agonists↗
PubMed1999

Effects of endothelin ET(B) receptor agonists and antagonists on the biphasic response in the ileum.

In the guinea-pig ileum, both sarafotoxin S6c and IRL1620 (Suc-[Glu9,Ala11,15]endothelin-1-(8-21) induced a concentration-dependent biphasic effect (relaxation and contraction), but distinct tachyphylaxis of the tissue. Cross-tachyphylaxis and additivity experiments evidenced distinct receptors for these agonists. BQ-123 (cyclo[D-Trp-D-Asp-Pro-D-Val-Leu]), an endothelin ET(A) receptor antagonist, did not affect the response induced by either agonist. PD145065 [Ac-(D-Bhg-Leu-Asp-Ile-Ile-Trp) (D-Bhg = 5H-dibenzyl[a,d]cycloheptene-10,11-dihydroglycine)], an endothelin ET(A)/ET(B) receptor antagonist, inhibited the contractions induced by IRL1620 and sarafotoxin S6c in competitive and noncompetitive manner, respectively. RES-701-1 [cyclic(Gly1-Asp9)(Gly-Asn-Trp-His-Gly-Thr-Ala-Pro-Asp-Trp-P he-Phe-Asn-Tyr-Tyr-Trp)], an endothelin ET(B1) receptor antagonist, inhibited both components of the response induced by IRL1620, whereas it inhibited mainly the relaxation induced by low sarafotoxin S6c doses. Apamin and suramin had different effects towards the agonists. Our results suggest that two endothelin ET(B) receptors with distinct signal transduction mechanism mediate the biphasic response: (1) the endothelin ET(B1) receptor: sensitive to RES-701-1 and PD145065 and (2) the endothelin ET(B2) receptor: less sensitive to RES-701-1 and PD145065.

Animals↗
PubMed1998

Inhibition of rat peritoneal mast cell exocytosis by frusemide: a comparison with disodium cromoglycate.

Among the loop diuretics, frusemide possesses unique airway protective activities which may be due to the inhibition of airway inflammatory cells such as the mast cell. We previously reported that frusemide and disodium cromoglycate (DSCG) demonstrated a similar profile of inhibitory activities against histamine release from rat peritoneal mast cells activated by various stimuli which increased intracellular calcium via different routes. Furthermore, the inhibitory activities of both compounds demonstrated marked tachyphylaxis and we hence postulated that frusemide and DSCG might share the same mechanism of action which involves the prevention of extracellular calcium influx into the mast cell cytoplasm. The present study confirmed the postulation by (a) demonstrating that cross-tachyphylaxis exists between the two compounds and (b) extending the observations on histamine release to the influx of extracellular calcium (45Ca) into rat peritoneal mast cells.

Animals↗
PubMed1985

Long refractory period after one application of nonimmunologic contact urticaria agents to the guinea pig ear.

The decrease in the swelling capacity and the length of the refractory period after nonimmunologic contact urticaria produced by one application of six human nonimmunologic contact urticaria agents was studied with the use of the guinea pig ear test. On retesting 1 day later, all substances (benzoic acid, cinnamic acid, cinnamic aldehyde, diethyl fumarate, methyl nicotinate, and dimethyl sulfoxide) showed reactions decreased by at least 50%. This decrease was most marked with cinnamic aldehyde (91% decrease), cinnamic acid (88%), and benzoic acid (86%). The tachyphylaxis was not specific to the substance producing it; reactivity to other contact urticaria agents decreased as well. The refractory period was 4 days after methyl nicotinate, 8 days after diethyl fumarate and cinnamic aldehyde, and 16 days after the other agents. These results suggest the following practical application: there is a need for (1) appropriate scheduling in the reuse of animals for testing for nonimmunologic contact urticaria and (2) an awareness of possible false-negative results in human tests for this form of urticaria because of tachyphylaxis.

Acrolein↗
PubMed1999

Insertion of an electronegative sulfur atom in the side chain of position 5 of angiotensin II: changes in the tachyphylactic properties of the peptide.

Angiotensin II (AII) analogs bearing n-Leu, Met or S-substituted groups for cysteine at position 5 were studied regarding their agonistic and tachyphylactic properties. It was shown that these analogs lowered the relative affinity towards the AT1 receptor as determined by contractile responses, which could be due to the removal of the beta-branching residue at position 5. Insertion of a sulfur atom in a different position away from the attached backbone carbon atom presented no significant difference in EC50 values for these analogs. Interestingly, the S-bearing analogs at position 5 were full agonists but the tachyphylactic property was lost, in contrast to [n-Leu5]AII, which still induced reduction of the contractile responses. Nevertheless after replacing the Asp with Sar in position 1 (Sar1) tachyphylaxis was again established. It is concluded that the insertion of Met or an S-substituted cysteine into the side chain at position 5 of AII may promote interactions with its receptor due to the slight electronegative character of the sulfur atom and changes in the restricted conformational freedom of the Ile5 residue in the AII molecule. This was overcome by Sar1, probably through interactions due to its fully protonated N-terminal amino group and favoring the conformation responsible for the tachyphylaxis phenomenon.

Amino Acid Substitution↗
PubMed1976

The effects of 2-phenylalanine 8-lysine vasopressin (octapressin) on blood vessels in the rat tail.

Isolated perfused segments of the ventral rat tail artery have been used in this study to investigate the effects of octapressin on vascular smooth muscle and its interaction with other vasoconstrictor agents. It was found that repeated octapressin administration was associated with tachyphylaxis and that the onset and rate of development of this phenomenon could be modified by cocaine. The constrictor action of catecholamines, electrical stimulation and serotonin on the rat tail artery was potentiated by octapressin. Mechanisms which may be involved in octapressin tachyphylaxis are discussed.

Angiotensin II↗
PubMed1987

Comparison of the inhibitory effects of antithrombin III, alpha 2-macroglobulin, and thrombin in human basilar arteries: relevance to cerebral vasospasm.

Isolated human basilar arteries were used in this study to evaluate the inhibitory effect of antithrombin III (AT III), thrombin, and alpha 2-macroglobulin (alpha 2-M) on contractions elicited by K+, serotonin (5-HT), prostaglandin (PG) D2, PGF2 alpha, and plasmin. alpha 2-M (0.5-1.0 mg/ml) failed to affect the contractions produced by contractile agonists significantly but did notably reduce the basal tone of the arteries. Thrombin (1 and 10 U/ml) reduced basal tone and significantly inhibited the contractions elicited by K+, PGF2 alpha, and plasmin. The relaxant effect of thrombin was abolished by procedures that destroy endothelium and by exposing the artery to thrombin for prolonged periods (tachyphylaxis). AT III (1-6 U/ml) reduced basal tone and significantly inhibited, in a concentration-dependent manner, the contractile responses to K+, 5-HT, PGD2, PGF2 alpha, and plasmin. In sharp contrast to thrombin, AT III did not induce tachyphylaxis nor was its vasorelaxant effect significantly reduced by destruction of the endothelium. The results show AT III to be a potent and nonspecific inhibitor of human cerebral arteries and support the hypothesis that AT III may contribute to the delay of cerebral vasospasm seen in patients who experience aneurysmal hemorrhage.

Adolescent↗
PubMed2001

Hydrogen peroxide induces a greater contraction in mesenteric arteries of spontaneously hypertensive rats through thromboxane A(2) production.

1. Hydrogen peroxide (H(2)O(2)) caused a transient contraction in endothelium-intact (E+) and -denuded (E-) mesenteric arteries (MA) from 8 - 10-month-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) in a concentration-dependent manner (10(-5) M to 10(-3) M). 2. The contraction to H(2)O(2) in MA (E+ or E-) was greater in SHR than in WKY. Removal of endothelium potentiated the contraction to H(2)O(2) in WKY but not in SHR. Tachyphylaxis to H(2)O(2) was less prominent in SHR than in WKY. 3. The contraction of aorta to H(2)O(2) (5 x 10(-4) M), expressed as a percentage of 80 mM KCl-induced contraction, was approximately half of that found in the MA. A greater contraction was found in E+ but not E- SHR aortic rings. 4. The contraction of MA to H(2)O(2) (5 x 10(-4) M) was greatly inhibited by SQ 29548 and ICI 192605 (thromboxane A(2) (TXA(2))/prostaglandin H(2) receptor antagonists), quinacrine (a phospholipase A(2) (PLA(2)) inhibitor), indomethacin and diclofenac (cyclooxygenase (COX) inhibitors), and furegrelate (a TXA(2) synthase inhibitor). 5. Production of thromboxane B(2) induced by H(2)O(2) (5 x 10(-4) M) was greater in SHR MA than in WKY, and was inhibited by quinacrine, indomethacin and diclofenac, and furegrelate, but not by SQ 29584 and ICI 192605. 6. These results suggested (1) that SHR MA exhibits a higher contraction involving an increased smooth muscle reactivity and less tachyphylaxis to H(2)O(2) than WKY; (2) that a greater production of TXA(2) through activation of PLA(2)-COX-TXA(2) synthase pathway appeared to be responsible for the enhanced contraction in SHR MA. The enhanced vascular response to H(2)O(2) may be related to hypertension in SHR.

Animals↗
PubMed2003

Mechanisms of sensitization of the response of single dorsal root ganglion cells from adult rat to noxious heat.

We investigated the regulation by nerve growth factor of the response of sensory neurons to noxious heat (>43 degrees C). In dissociated dorsal root ganglion neurons (<30 micro m) from adult rat we demonstrated, using perforated patch clamp recording, that the inward current elicited in response to noxious heating is enhanced by nerve growth factor and reduced by capsazepine. The tachyphylaxis observed in response to the second of two heat pulses was reversed in most cells when nerve growth factor was introduced into the medium during the 5 min between the two heat stimuli, similar to findings using capsaicin [X. Shu & L.M. Mendell (1999) Neurosci. Lett.274, 159-162]. The threshold temperature did not change systematically after nerve growth factor. Using antibodies to TRPV1 and trkA in a subset of cells from which we recorded, we found a virtually perfect correlation between expression of TRPV1 and sensitivity to noxious heat. In addition, trkA expression was perfectly correlated with the ability of nerve growth factor to reverse tachyphylaxis. Thus, this physiological test is a reliable measure of trkA expression in cells sensitive to noxious heat. In agreement with studies in heterologous cells expressing trkA and TRPV1, pharmacologically blocking phospholipase C abolished the effect of nerve growth factor on heat-evoked currents in cells verified to express trkA. We conclude that the response of dorsal root ganglion neurons to noxious heat is conditioned by nerve growth factor in the same way as their response to capsaicin and that these responses require the presence of trkA and TRPV1.

Animals↗