Modification of tumour blood flow using the hypertensive agent, angiotensin II

Tozer, G. M.; Shaffi, KM

doi:10.1038/bjc.1993.180

Cited by 38 publications

(37 citation statements)

References 24 publications

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“…Early generations of the P22 transplanted rat carcinosarcoma were grown subcutaneously in the left flank of 10-to 12-week-old male BDIX rats as described previously (Tozer and Shaffi, 1993). Tumours were used for experiments when they reached 1 -2 g (all three orthogonal diameters 10 -15 mm, including the skin thickness).…”

Section: Animals and Tumoursmentioning

confidence: 99%

“…The experimental procedure for the determination of blood flow using 14 C-labelled iodoantipyrine ( 14 C-IAP) (Amersham Life Sciences, UK) and 125 I-labelled iodoantipyrine ( 125 I-IAP) (Institute of Cancer Research, Sutton, UK) has been described previously (Tozer and Shaffi, 1993). In brief, rats were anaesthetised and kept warm, as described above.…”

Section: Blood Flowmentioning

confidence: 99%

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The endothelin B (ETB) receptor agonist IRL 1620 is highly vasoconstrictive in two syngeneic rat tumour lines: potential for selective tumour blood flow modification

et al. 2005

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The vascular effects of the endothelin B (ET B ) receptor agonist IRL 1620 were investigated in the rat P22 carcinosarcoma and a range of normal tissues in BDIX rats. Tissue blood flow rate was calculated from measurements of tissue uptake of radiolabelled iodoantipyrine. A comparison of vascular effects in the P22 tumour and the HSN sarcoma growing in CBH/CBi rats was made using laser Doppler flowmetry, showing similar effects of IRL 1620, with red cell flux rapidly decreasing by 50 -60% and then returning to control levels within approximately 30 min. This corresponded to similar levels but different spatial organisation of ET B binding sites in the two tumours, as measured by autoradiography. The decrease in tumour blood flow and an increase in vascular resistance suggest that the vascular component of ET B receptors in the P22 tumour is localised on contractile elements rather than on endothelial cells. ET A receptors were also identified. Vasoconstriction occurred uniformly throughout the P22 tumour mass, consistent with a measured homogeneous distribution of ET B receptors. IRL 1620 caused vasoconstriction in normal skeletal muscle, kidney and small intestine of the BDIX rat as well as in tumour, but did not affect blood flow in other tissues. These effects could be useful for limiting toxicity of certain chemotherapeutic agents. Fully functional ET B receptors are clearly expressed on tumour vasculature and IRL 1620 shows promise for short-term modification of tumour blood flow. Expression levels of ET B receptors on the tumour vasculature could be useful for predicting which tumours are likely to respond to IRL 1620.

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Section: Animals and Tumoursmentioning

confidence: 99%

Section: Blood Flowmentioning

confidence: 99%

The endothelin B (ETB) receptor agonist IRL 1620 is highly vasoconstrictive in two syngeneic rat tumour lines: potential for selective tumour blood flow modification

et al. 2005

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“…B16F1 mouse melanoma ( CRL6323; American Type Culture Collection, Manassas, VA ), P22 rat carcinosarcoma, 16 SaF mouse sarcoma, 17 and T24 human bladder carcinoma ( European Collection of Cell Cultures, Ref. no.…”

Section: Cell Lines and Tumor Modelsmentioning

confidence: 99%

Effective gene transfer to solid tumors using different nonviral gene delivery techniques: Electroporation, liposomes, and integrin-targeted vector

et al. 2002

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In this study, we measured transfection efficiency in vitro and in vivo using the following nonviral approaches of gene delivery: injection of plasmid DNA, electroporation -assisted, liposome -enhanced, and integrin -targeted gene delivery, as well as the combination of these methods. Four histologically different tumor models were transfected with a plasmid encoding the green fluorescent protein ( GFP ) ( B16 mouse melanoma, P22 rat carcinosarcoma, SaF mouse sarcoma, and T24 human bladder carcinoma ) using adherent cells, dense cell suspensions, and solid tumors. Emphasis was placed on different electroporation conditions to optimise the duration and amplitude of the electric pulses, as well as on different DNA concentrations for effective gene delivery. In addition, transfection efficiency was correlated with cell density of the tumors. The major in vivo findings were: ( a ) electroporationassisted gene delivery with plasmid DNA, employing long electric pulses with low amplitude, yielded significantly better GFP expression than short electric pulses with high amplitude; ( b ) electroporation combined with liposome -DNA complexes yielded the highest percentage of transfected tumor area in B16F1 tumor ( 6% ); ( c ) transfection efficiency of electroporation -assisted plasmid DNA delivery was dependent on tumor type; ( d ) integrin -targeted vector, alone or combined with electroporation, was largely ineffective. In conclusion, our results demonstrate that some nonviral methods of gene delivery are feasible and efficient in transfecting solid tumors. Therefore, this makes nonviral methods attractive for further development.

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“…Here, we report on the effects of AMD6245 and AMD6221 on the growth and vascularization of a rat carcinosarcoma P22 (35). We have compared the results with those obtained using N G -nitro-L-arginine methyl ester (L-NAME), a nonselective NOS inhibitor, and with AG and 1400W, both of which display greater selectivity for NOS II than for NOS III (13,14).…”

Section: Introductionmentioning

confidence: 99%

Antitumor Actions of Ruthenium(III)-Based Nitric Oxide Scavengers and Nitric Oxide Synthase Inhibitors

Flitney

Pritchard²,

Kennovin³

et al. 2011

Molecular Cancer Therapeutics

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The role of endogenous nitric oxide (NO) in the growth and vascularization of a rat carcinosarcoma (P22) has been investigated. Tumor-bearing animals were treated with (i) nitric oxide synthase (NOS) inhibitors, administered via the drinking water, including N G -nitro-L-arginine methyl ester (L-NAME), a nonisoform-selective inhibitor, and 2 others that target the inducible (NOS II) enzyme preferentially, namely 1-amino-2-hydroxyguanidine or N-[3-(aminomethyl)benzyl]acetamidine hydrochloride; or (ii) daily injections (intraperitoneally) of 2 Ru(III) polyaminocarboxylates, AMD6221 and AMD6245, both of which are effective NO scavengers. L-NAME, AMD6221, and AMD6245 reduced tumor growth by approximately 60% to 75% of control rates. Tumor sections stained with abs to CD-31/platelet endothelial cell adhesion molecule-1 or NOS III showed that this was associated with a marked reduction (60%-77%) of tumor microvascular densitiy (MVD). Tumors resumed growing promptly when treatment was discontinued, accompanied by partial or complete restoration of MVDs. In contrast, NOS-II selective inhibitors had no effect on tumor growth or vascularization, indicating that both responses require complete blockade of NO production. The results corroborate the view that endogenous NO facilitates tumor development. We suggest that NO deprivation causes tumor feeder vessels to constrict, reducing tumor blood flow. The delivery of oxygen and essential nutrients to the developing tumor is impaired as a consequence, hampering further growth. Normalizing NO levels by withholding treatment causes tumor feeder vessels to dilate, increasing tumor perfusion and reestablishing conditions that allow tumors to begin growing again.

show abstract

Modification of tumour blood flow using the hypertensive agent, angiotensin II

Cited by 38 publications

References 24 publications

The endothelin B (ETB) receptor agonist IRL 1620 is highly vasoconstrictive in two syngeneic rat tumour lines: potential for selective tumour blood flow modification

The endothelin B (ETB) receptor agonist IRL 1620 is highly vasoconstrictive in two syngeneic rat tumour lines: potential for selective tumour blood flow modification

Effective gene transfer to solid tumors using different nonviral gene delivery techniques: Electroporation, liposomes, and integrin-targeted vector

Antitumor Actions of Ruthenium(III)-Based Nitric Oxide Scavengers and Nitric Oxide Synthase Inhibitors

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