Endothelium enhances tachyphylaxis to angiotensins II and III in rat aorta

Gruetter, Carl A.; Ryan, Errol T.; Schoepp, Darryle D.

doi:10.1016/0014-2999(87)90745-x

Cited by 25 publications

(10 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, these observations conflict with studies from one of our laboratories, which found no effect on Ang II responsiveness of rabbit thoracic aorta by denudation of the endothelium or by a number of EDRF inhibitors (8). Despite this conflict between our previous studies and the observations by Yilmaz et al, several additional explanations may be considered for the absence of augmentation of Ang II responsiveness by EDRF antagonists in our cyclooxygenase inhibited preparation: (a) there may be differences in reactivity between systemic and pulmonary vessels and between whole blood perfused vascular beds and larger vessels studied in ring preparations; and (b) it is unclear why the vehicles alone heightened Ang II constriction in this study, but may be related to endothelium-independent mechanisms directly involving the vascular smooth muscle (36). Nevertheless, this effect of the vehicles may have masked further potentiation of Ang II vasoconstriction by the putative EDRF antagonists.…”

Section: Discussionmentioning

confidence: 87%

Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.

Brashers¹,

Peach²,

Rose³

1988

J. Clin. Invest.

131

View full text Add to dashboard Cite

The role of the endothelium in hypoxic constriction of the intact pulmonary vascular bed has not been clearly elucidated.To test for a possible role for endothelium-derived relaxing factor(s) (EDRF) in the hypoxic pressor response, isolated, whole blood-perfused rat lungs from male Sprague-Dawley rats treated with meclofenamate were prepared. Three protocols were performed, including: (a) normal saline (control); (b) the putative EDRF inhibitors, eicosatetraynoic acid (ETYA, 1 X 10-4 M) or nordihydroguaiaretic acid (NDGA, 1 X 10-4 M) versus vehicle DMSO; and (c) the putative EDRF inhibitor hydroquinone (HQ, 1 X 10-4 M) versus vehicle ethyl alcohol (ETOH). The pulmonary pressor response to angiotensin II (Ang II, 0.25 Mg) injections alternated with 6-min periods of hypoxic ventilation (3% 02,5% C02) was measured before and after the administration of saline, inhibitors, or vehicles. The administration of the EDRF inhibitors ETYA, NDGA, and HQ resulted in a marked accentuation of the hypoxic pressor response that was not seen in the controls (P < 0.05). In separate experiments, lungs precontracted with norepinephrine (1 X 10-6 M) were pretreated with edrophonium (1 X 10-4 M) and then observed for endothelium-dependent vasodilator responses to acetylcholine at increasing doses (1 X 10-7 X 10-4 M). Administration of ETYA, NDGA, or HQ abrogated the observed vasodilatation to acetylcholine, which was not seen with vehicles alone (P < 0.01). These studies suggest an important role for the endothelium in pulmonary vascular responsiveness to alveolar hypoxia through possible release of a relaxing factor(s) that attenuates the degree of pulmonary arterial constriction.

show abstract

Section: Discussionmentioning

confidence: 87%

Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.

Brashers¹,

Peach²,

Rose³

1988

J. Clin. Invest.

131

View full text Add to dashboard Cite

show abstract

“…In endothelium-denuded rat aortic ring preparations, the E,., value of the second CRC for All was much less than that of AIII and AIV, indicating that the endothelium appears to be less influential on AII-induced tachyphylaxis. Although two mechanisms (endothelium-dependent and endothelium-independent) may be involved in the development of the tachyphylaxis to angiotensin (Gruetter et al, 1987), the details remain unclear.…”

Section: -3mentioning

confidence: 99%

Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Zhang

Pfaffendorf

et al. 1995

British J Pharmacology

View full text Add to dashboard Cite

1 In the present study, the contractile effects of angiotensin III (AIII) and angiotensin IV (AIV) compared with those of angiotensin II (AII) were determined in rat aortic ring preparations. 2 All three peptides caused concentration-dependent contractions with similar maximal responses. AIII proved approximately 4 times less potent than AII, whereas AIV was about 1000 times less active than AIL.3 The selective AT,-receptor antagonist, losartan (10-300 nM) caused parallel rightward shifts of the concentration-response curves (CRC) for all three peptides. The Schild plot slopes for the effect of losartan on AIII curves were significantly lower than unity (P<0.05). The selective AT2-receptor antagonist, PD123177 did not influence the CRCs for AII and AIV. However, the AIII curves were moderately shifted leftward in the presence of PD123177 (0.1 and 1 JiM).4 Destruction of the endothelium or incubation with the NO-synthesis inhibitor N0-monomethyl-Larginine acetate (L-NMMA) (0.1 mM) significantly enhanced the contractile responses to all three peptides. 5Tachyphylaxis was investigated by constructing a second CRC for all three peptides, after an interval of 1 h. The presence of endothelium significantly enhanced the development of tachyphylaxis to all three peptides. However, in endothelium-denuded preparations, the E,,,,,, value of the second curve elicted by AII was about 50%, compared with the first one, whereas for AIII and AIV E,,,, values were as high as 90% and 100%, respectively. 6 Our results indicate that both AIII and AIV are less potent but similarly efficacious vasoconstrictor agents compared with AII. Their contractile effects are also mediated by AT,-receptors and probably modulated by endothelium. Tachyphylaxis induced by AIII and AIV proved weaker than that for AII. Tachyphylaxis appears to be enhanced by the presence of an intact endothelium.

show abstract

“…Since AII-induced tachyphylaxis was first recognised (Page & Helmer 1940), the phenomenon has been extensively studied using mainly in vitro preparations (Khairallah et al 1966;Paiva 1977;Gruetter et al 1987;Oshiro et al 1989). In vivo studies on AII-induced tachyphylaxis are difficult to perform and the existence of the phenomenon in intact preparations has not been fully established ).…”

mentioning

confidence: 99%

Effects of Noradrenaline and Prostaglandin F_2α on Angiotensin‐Induced Contraction and Tachyphylaxis in Rat Aortic Rings

Kuttan

1992

Pharmacology & Toxicology

View full text Add to dashboard Cite

The aim of this study was to examine the effects of noradrenaline (NA) and prostaglandin F2 alpha (PGF2 alpha) on angiotensin II (AII)-induced contraction and tachyphylaxis in aortic rings of the rat. Neither NA (10(-9) M) nor PGF2 alpha (10(-7) M) had significant effect on the response of the rings to the spasmogenic concentrations (10(-10) to 10(-7) M) of AII, but lowered significantly the threshold response of the aortic rings to AII (from 10(-9) to 10(-12) M). In rings that were tachyphylatic to AII, both NA and PGF2 alpha attenuated significantly the tachyphylaxis of the rings to AII at the concentrations of 10(-10) and 10(-7) of the octapeptide; and also lowered the threshold of the tachyphylatic rings to AII (from 10(-9) to 10(-11) M for NA, and from 10(-9) to 10(-10) M for PGF2 alpha). The specific properties of noradrenaline and PGF2 alpha were not shared by the non-specific potassium chloride. Because the lowering of threshold and attenuation of tachyphylaxis occurred at the physiological levels of AII and NA, it is possible that the in vivo actions of AII are under constant modulation by circulating and localised (higher than circulating) levels (e.g. of PGF2 alpha) of spasmogens. The results also call into question the physiological significance of angiotensin tachyphylaxis and may suggest that it is only an in vitro phenomenon occurring in the absence of endogeneous spasmogens.

show abstract

Endothelium enhances tachyphylaxis to angiotensins II and III in rat aorta

Cited by 25 publications

References 5 publications

Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.

Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.

Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Effects of Noradrenaline and Prostaglandin F_2α on Angiotensin‐Induced Contraction and Tachyphylaxis in Rat Aortic Rings

Contact Info

Product

Resources

About

Endothelium enhances tachyphylaxis to angiotensins II and III in rat aorta

Cited by 25 publications

References 5 publications

Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.

Augmentation of hypoxic pulmonary vasoconstriction in the isolated perfused rat lung by in vitro antagonists of endothelium-dependent relaxation.

Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta

Effects of Noradrenaline and Prostaglandin F2α on Angiotensin‐Induced Contraction and Tachyphylaxis in Rat Aortic Rings

Contact Info

Product

Resources

About

Effects of Noradrenaline and Prostaglandin F_2α on Angiotensin‐Induced Contraction and Tachyphylaxis in Rat Aortic Rings