Modification of tumor blood flow and enhancement of therapeutic effect of ACNU on experimental rat gliomas with angiotensin II

Tokuda, Kouichi; Abe, Hiroshi; Aida, Toshimitsu; Sugimoto, Shin-ichiro; Kaneko, Satoshi

doi:10.1007/bf00177353

Cited by 14 publications

(5 citation statements)

References 16 publications

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“…Besides, RAS inhibiting agents have shown promising benefits in the management of end-organ damage, ischemia, atherosclerosis, and cardiovascular-related disease (Nehme, 2019). A timeline of key historical findings associated with the study and discovery of Ang II associated with RAS is shown in Table 1 (Burton et al, 1985;Gibbons, 1998;Basso and Terragno, 2001;Andrea et al, 2006;Atlas, 2007;Skrbic and Igic, 2009;Benigni et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update

et al. 2021

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The multifaceted nature of the renin-angiotensin system (RAS) makes it versatile due to its involvement in pathogenesis of the cardiovascular disease. Angiotensin II (Ang II), a multifaceted member of RAS family is known to have various potential effects. The knowledge of this peptide has immensely ameliorated after meticulous research for decades. Several studies have evidenced angiotensin I receptor (AT1 R) to mediate the majority Ang II-regulated functions in the system. Functional crosstalk between AT1 R mediated signal transduction cascades and other signaling pathways has been recognized. The review will provide an up-to-date information and recent discoveries involved in Ang II receptor signal transduction and their functional significance in the cardiovascular system for potential translation in therapeutics. Moreover, the review also focuses on the role of stem cell-based therapies in the cardiovascular system.

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Section: Introductionmentioning

confidence: 99%

An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update

et al. 2021

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“…Later, Jirtle et al (1978) found that constant intravenous infusion of high dose angiotensin 11 (1.4 Ag min ') into tumour-bearing rats caused a 4-fold increase in blood flow to the tumour growing in the mammary gland relative to that in the normal mammary gland and skin although the absolute blood flow to the tumour was decreased from 1.3 ml g -min ' to 0.8 ml g' min-'. Subsequent studies have shown that angiotensin IIinfusion can increase absolute, as well as relative, blood flow in some tumour systems (Tokuda et al, 1990;Hori et al, 1991;Tanda et al, 1991;Trotter et al, 1991).…”

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confidence: 99%

“…Figure 8 shows Mean arterial blood pressure (mmHg) 0.6 of the control value (P = 0.02) but not at all in sections cut from the tumour centre (P = 0.54). Thus the blood flow elatonshpbewee anitni I *idue inreae reduction to 0.8 of the control value in whole tumours pressure and the coefficient of variation for blood efficient of variation was calculated from the means (Figure 4) Mean arterial blood pressure (mmHg) Figure 8 Comparison , Tokuda et al, 1990. The reasons for this discrepancy are unclear.…”

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confidence: 99%

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

Tozer

Shaffi²

1993

Br J Cancer

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Summary The effects of different doses of angiotensin 11 (0.02 to 0.5 jlg kg-' min-' on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 12511 or 4C-labelled iodoantipyrine ('25I-IAP and '4C-IAP). Spatial heterogeneity of blood flow within tumours, before and after angiotensin II infusion, was also measured using '4C-IAP and an autoradiographic procedure. Mean arterial blood pressure rose steeply with angiotensin II dose. Blood flow to skeletal muscle, skin overlying the tumour, contralateral skin, small intestine and kidney tended to decline in a dose-dependent manner. Blood flow to the tumour was also reduced (to 80% of control values) but there was no dose response. Blood flow to the heart was slightly increased and blood flow to the brain was unaffected by angiotensin II. Vascular resistance, in all tissues, was increased by angiotensin II infusion. The increase in tumour tissue was similar to that found in skeletal muscle and small intestine and is likely to be caused by a direct vasoconstricting effect of the drug rather than autoregulation of tumour blood flow in the face of an increase in perfusion pressure. The reduction in overall blood flow at the highest perfusion pressure was due to a preferential effect of angiotensin II at the tumour periphery. These results show that some tumours, at least, can respond directly to the effects of vasoactive agents.

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“…The use of AT II as a strong vasoconstrictor led to non-uniform results. In some studies AT II resulted in a passive expansion of the vascular bed due to the increased perfusion pressure (Hori et al, 1985;, an increase in tumour perfusion (Shankar et al, 1999;Suzuki et al, 1981;1984;Tokuda et al, 1990;Trotter et al, 1991), as well as a reduction in the fraction of transiently occluded microvessels (Hemingway et al, 1992;Trotter et al, 1991). In contrast, other studies showed a decrease in tumour perfusion during systemic application of AT II (Dworkin et al, 1997;Jirtle et al, 1978;Tozer and Shaffi, 1993;Tozer et al, 1996).…”

Section: Discussionmentioning

confidence: 91%

Disparate responses of tumour vessels to angiotensin II: tumour volume-dependent effects on perfusion and oxygenation

2000

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Summary Perfusion and oxygenation of experimental tumours were studied during angiotensin II (AT II) administration whereby the rate of the continuous AT II infusion was chosen to increase the mean arterial blood pressure (MABP) by 50-70 mmHg. In subcutaneous DSsarcomas the red blood cell (RBC) flux was assessed using the laser Doppler technique and the mean tumour oxygen partial pressure (pO 2 ) was measured polarographically using O 2 -sensitive catheter and needle electrodes. Changes in RBC flux with increasing MABP depended mainly on tumour size. In small tumours, RBC flux decreased with rising MABP whereas in larger tumours RBC flux increased parallel to the MABP. As a result of these volume-dependent effects on tumour blood flow, the impact of AT II on tumour pO 2 was also mainly tumour volume-related. In small tumours oxygenation decreased with increasing MABP during AT II infusion, whereas in large tumours a positive relationship between blood pressure and O 2 status was found. This disparate behaviour might be the result of the co-existence of two functionally distinct populations of tumour vessels. In small tumours, perfusion decreases presumably due to vasoconstriction of pre-existing host vessels feeding the tumour. In larger malignancies, newly formed tumour vessels predominate and seem not to have this vasoresponsive capability (lack of smooth muscle cells and/or AT receptors), resulting in an improvement of perfusion which is not tumour-related per se, but is due to the increased perfusion pressure.

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Modification of tumor blood flow and enhancement of therapeutic effect of ACNU on experimental rat gliomas with angiotensin II

Cited by 14 publications

References 16 publications

An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update

An Insight on Multicentric Signaling of Angiotensin II in Cardiovascular system: A Recent Update

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

Disparate responses of tumour vessels to angiotensin II: tumour volume-dependent effects on perfusion and oxygenation

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