Angiotensin II-induced tachyphylaxis in aortas of normo- and hypertensive rats: changes in receptor affinity

Kuttan, S.C.

doi:10.1016/0014-2999(93)90771-9

Cited by 24 publications

(20 citation statements)

References 14 publications

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“…However, because AngII releases PG from a variety of blood vessels 8,9 and PG such as PGE 1 , E 2 , A 1 and A 2 are potent dilators of veins in humans, 23 vasodilatory PG may contribute to rapid desensitization of responses to AngII. Some in vitro studies 11,12 support this idea. However, no in vivo data are available regarding the involvement of PG in this phenomenon in humans.…”

Section: Discussionmentioning

confidence: 89%

Angiotensin Ii in Human Veins: Development of Rapid Desensitization and Effect of Indomethacin

Harada

Ohmori

Kitoh

et al. 1999

Clin Exp Pharma Physio

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SUMMARY 1. The present study investigated whether rapid desensitization (tachyphylaxis) develops after exposure of human hand veins to angiotensin (Ang)II and whether pretreatment with indomethacin affects its development. 2. Venoconstrictor responses to increasing (2–256 ng/min) and constant (50 ng/min) doses of AngII and noradrenaline (NA) infusion were obtained in six healthy male subjects using the dorsal hand vein technique. After pretreatment with indomethacin and placebo, venoconstrictor responses to 50 ng/min AngII infusion were obtained in eight healthy male subjects. 3. The maximal mean (±SD) venoconstrictor response to NA (obtained with 256 ng/min NA) was 93.1±4.7%, whereas that to AngII (obtained with doses between 16 and 128 ng/min) was 43.8±12.2%. Continuous infusion of NA induced constant venoconstriction, whereas the venoconstrictor response to AngII peaked 3 min after the beginning of infusion and, thereafter, was attenuated. 4. Venoconstriction in response to constant AngII infusion after indomethacin pretreatment was significantly larger than that after placebo from 6 to 18 min after the initiation of infusion. 5. These findings show that rapid desensitization to AngII develops in human hand veins and this is compatible with the hypothesis that vasodilator prostaglandins are involved in the development of this desensitization.

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Section: Discussionmentioning

confidence: 89%

Angiotensin Ii in Human Veins: Development of Rapid Desensitization and Effect of Indomethacin

Harada

Ohmori

Kitoh

et al. 1999

Clin Exp Pharma Physio

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“…In an animal aortic strip, Ang II concentration contractile response curves were highly reproducible, and tachyphylaxis to the contractile response elicited by Ang II could be induced by repeated exposure [33,34]. Tachyphylaxis to Ang II in rabbit isolated aorta is modulated by an AT1 receptor antagonist [34], and Ang II tachyphylaxis also occurs in the guinea pig ileum [35].…”

Section: Discussionmentioning

confidence: 99%

Importance of the Angiotensin Type 1 Receptor in Angiotensin Ii–induced Bronchoconstriction and Bronchial Hyperresponsiveness in the Guinea Pig

Watanabe

Myou

Fujimura

et al. 2004

Experimental Lung Research

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Although angiotensin II (Ang II) causes bronchoconstriction and bronchial hyperresponsiveness to methacholine in mildly asthmatic patients, the responsible mechanisms for these reactions are unclear. The authors examined the effect of intravenous infusion of Ang II on airway constriction in guinea pigs. Furthermore, the effects of subthreshold concentrations of Ang II on bronchial responsiveness to methacholine were investigated. Airway opening pressure (Pao), an index of bronchoconstriction, increased dose dependently after intravenous infusion of 3 and 10 nmol/kg Ang II (72.2 and 236.5 increase above the baseline value, respectively). In another set of experiments, animals received a methacholine inhalation challenge under a constant intravenous infusion of a subthreshold dose of Ang II (2 nmol/kg/min). The Ang II infusion elicited bronchial hyperresponsiveness to methacholine. The provocative concentration of methacholine, which produced a 200% increase above the baseline Pao (PC200), decreased from 306.9 to 156.1 micrograms/mL upon Ang II infusion. Pretreatment with TCV-116, a type 1 Ang II (AT1) receptor antagonist, but not PD123319, a type 2 Ang II (AT2) receptor antagonist, dose dependently prevented both the Ang II-induced bronchoconstriction and bronchial hyperresponsiveness to methacholine. The authors conclude that Ang II caused bronchoconstriction and induced bronchial hyperresponsiveness to methacholine via the AT1 receptors and that this effect did not involve the release of other bronchoactive mediators.

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“…Abdellatif et al, 1991;Kuttan & Sim, 1993;Reagan et al, 1993). It should be noted, however, that the time course of the apparent desensitization of the response was markedly different between the two preparations and it could not be ruled out that at least a component of the apprent desensitization was due to a depletion of neuronal dopamine levels.…”

Section: Stereotaxic Implantation Of Chronic Indwelling Guide Cannulaementioning

confidence: 97%

Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo

Brown

Steward

Jin

et al. 1996

British J Pharmacology

105

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1 The ability of angiotensin II to modulate dopamine release from rat striatal slices in vitro and in the intact rat striatum in vivo was assessed by the microdialysis technique.2 In slices of rat striatum, angiotensin II (0.1-1.0 gM) induced a concentration-related increase in endogenous dopamine release which was maximal (approximately 250% above basal levels) within the first 2-4 min of agonist application and subsequently declined to near

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Angiotensin II-induced tachyphylaxis in aortas of normo- and hypertensive rats: changes in receptor affinity

Cited by 24 publications

References 14 publications

Angiotensin Ii in Human Veins: Development of Rapid Desensitization and Effect of Indomethacin

Angiotensin Ii in Human Veins: Development of Rapid Desensitization and Effect of Indomethacin

Importance of the Angiotensin Type 1 Receptor in Angiotensin Ii–induced Bronchoconstriction and Bronchial Hyperresponsiveness in the Guinea Pig

Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo

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Angiotensin II-induced tachyphylaxis in aortas of normo- and hypertensive rats: changes in receptor affinity

Cited by 24 publications

References 14 publications

Angiotensin Ii in Human Veins: Development of Rapid Desensitization and Effect of Indomethacin

Angiotensin Ii in Human Veins: Development of Rapid Desensitization and Effect of Indomethacin

Importance of the Angiotensin Type 1 Receptor in Angiotensin Ii–induced Bronchoconstriction and Bronchial Hyperresponsiveness in the Guinea Pig

Ability of angiotensin II to modulate striatal dopamine release via the AT1 receptor in vitro and in vivo

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Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo