Effects of Angiotensin II and Some Analogues on Vascular Permeability in the Rabbit

Robertson, Abel L.; Khairallah, Philip A.

doi:10.1161/01.res.31.6.923

Cited by 127 publications

(34 citation statements)

References 12 publications

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“…In the present experi mental conditions, inhibitors of the renin-angio tensin system were administered systemically, and the presence of the blood-brain barrier may limit the movements of these compounds into the brain. However, this barrier is known to be disrupted under conditions of ischemia (Ito et aI., 1976;Ra poport, 1976;Chui et aI., 1981), and thus, the overall permeability could be increased not only to circulating angiotensin II, but also to the infused compounds (Robertson and Khairallah, 1972). Even if the barrier is not disrupted, these com pounds could be acting on brain structures located outside the blood-brain barrier (Ganong, 1984) or, most likely, the vessels themselves.…”

Section: Discussionmentioning

confidence: 99%

Differences in Mortality Rate between Abrupt and Progressive Carotid Ligation in the Gerbil: Role of Endogenous Angiotensin II

Kaliszewski

Fernandez²,

Wicke³

1988

J Cereb Blood Flow Metab

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Summary: Studies have shown that in comparison to rapid occlusion of a vessel, gradual occlusion produces less severe tissue ischemia due to a more effective devel opment of collateral circulation. As other studies have shown that collateral circulation can be enhanced by stimulation of the endogenous renin-angiotensin II system, it was hypothesized that this system is involved in the mechanism of protection against ischemia that ob tains during gradual vascular occlusion. To test this hy pothesis, mortality rates were evaluated in gerbils sub jected to gradual vascular occlusion by means of progres sive carotid ligation while simultaneously infused with inhibitors of the renin-angiotensin II cascade-enala prilat or saralasin. Groups of animals with either abrupt or progressive carotid ligation infused with saline served as controls. Results showed that (1) in saline-infused anGradual occlusion of a vessel results in a less de leterious effect on the tissue elements of the distal territory in comparison to an abrupt occlusion. This difference is due to the presence of adaptive mech anisms that require time to be engaged and cannot be properly utilized when the occlusion is made quickly. As a result of these adaptive mechanisms, a more effective development of collateral circula tion occurs that reduces the severity of tissue isch emia. This effect can be seen not only in the arterial side of circulation, such as cerebral or coronary ar teries (Svarzbein et aI. , 1974; To moike et aI., 1981;Bache and Schwartz, 1983; Patterson et aI. , 1983), but also in the venous side such as the portal vein Received September 30, 1986; accepted October 21, 1987. Address correspondence and reprint requests to Dr. Leonardo A. Fernandez, at Section of Neurosurgery, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510, U.S.A. 149imals, there was a significant decrease in the mortality rate of progressive-ligated animals when compared to abrupt-ligated animals, and (2) administration of either enalaprilat or saralasin to progressive-ligated animals re sulted in mortality rates that were indistinguishable from those of saline-infused abrupt-ligated animals. These re sults suggest that the endogenous renin-angiotensin system is indeed involved in an adaptive mechanism that occurs during progressive ligation of the carotid artery, and more specifically, that the relatively benign effect of progressive carotid ligation may be due to the action of angiotensin II to stimulate the development of collateral circulation and reduce the severity of focal brain isch emia.

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Section: Discussionmentioning

confidence: 99%

Differences in Mortality Rate between Abrupt and Progressive Carotid Ligation in the Gerbil: Role of Endogenous Angiotensin II

Kaliszewski

Fernandez²,

Wicke³

1988

J Cereb Blood Flow Metab

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“…Since nitroglycerin reduces the venous return (= preload) and directly decreases the vascular resistance of arteries (= afterload), it is theoretically reasonable that nitroglycerin has a preventive effect on the development of AT II-induced pulmonary edema (9,10). Since the development of PE is probably due not only to elevated afterload in the systemic circulation but also to hyperpermeability in the pulmonary vascular beds (11), it is reasonable to discuss the preventive effect of AT II receptor antagonists on the changes in the afterload (12,13) and the pulmonary vascular permeability (14). As regards to the increased afterload caused by AT II, our experiments showed that only E 4177 could suppress the elevation of blood pressure after administering AT II.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Edema Induced by Angiotensin II in Rats

Shimakura

Sanaka

Wang

et al. 1995

Japanese Journal of Pharmacology

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ABSTRACT-Weperformed this study to demonstrate the experimental procedure for inducing pulmonary edema by angiotensin II (AT II) in rats and to determine the mechanism of hemodynamic pulmonary edema. In the pilot study, 10 pg/ml of AT II was found to be adequate as the edematogenic dose for inducing pulmonary edema. The edematogenic dose of AT II was intravenously given to rats pretreated with 20 mg/kg of an AT II-receptor antagonist, E 4177 (3-[(2"-carboxybiphenyl-4-yl)methyl]-2-cyclopropyl-7-methyl-3H-imidazo [4,5-b]pyridine), and to rats given 10 mg/kg of an alpha-adrenergic blocker, phentolamine. Similarly, pulmonary edema was induced by 25 tcg/ml of adrenaline in rats pretreated with E 4177 (20 mg/kg) and rats with no pretreatment. E 4177 completely suppressed the development of AT II-induced pulmonary edema, whereas phentolamine could not. On the contrary, E 4177 could not suppress the development of adrenaline-induced pulmonary edema. We concluded that AT II-induced pulmonary edema will develop via the specific AT II receptor without the indirect action of adrenaline.Keywords: Pulmonary edema, Angiotensin II, Adrenaline, Angiotensin II-receptor antagonist, PhentolamineHeart failure causes an increase in systemic vascular resistance and an accumulation of excess fluid as the compensatory adaptations of enhanced activities of the sympathetic nervous system and the renin-angiotensin system. The clinical features relating to pulmonary edema arise in the end-stage of the left ventricular failure due to the excessive compensatory adaptations.Angiotensinconverting enzyme inhibitors have currently attracted the attention of physicians as effective drugs that improve the prognostic outcomes of patients with heart failure (1). Since the drugs suppress the production of angiotensin II (AT II) which has a vigorously vasoconstrictive effect, they bring about a favorable clinical course in those patients. Although many studies have established experimentally that high doses of adrenaline, one of the most powerful cardiac stimulants, induce pulmonary edema as the result of increased afterload in systemic circulation which elevates the left atrial pressure (2), there are no reports to our knowledge, on the experimental induction of pulmonary edema by AT II. In the course of the study on pulmonary edema, we had been concerned with the vasoconstrictive effect of AT II and found that the bolus intravenous injection of AT II also induced pulmonary edema in rats. We therefore undertook the present study for the following reasons: 1) to propose the experimental procedure for inducing pulmonary edema by the administration of AT II in rats and 2) to determine the mechanism of AT II-induced pulmonary edema and the protective measures against it. MATERIALS AND METHODS Animals and outline of the experimentMale albino rats of the Wistar strain (n=57) weighing 250-300 g were purchased from Saitama Animal Lab.(Saitama) and housed under controlled conditions for at least two weeks before the experiments. They were randomly divided into...

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“…A wide variety of biologic activities has been attributed to angiotensin II, including hemodynamic effects such as elevation of blood pressure (15), decreased mesenteric blood flow in cats, dogs, and humans (16)(17)(18)(19), and reduced blood flow and vasoconstriction in perfused limbs of rabbits, cats and dogs (16,20). Angiotensin II enhances vascular permeability (21,22) and induces widening of interendothelial cell spaces in aortic, coronary, mesenteric, and peripheral arteries (16,21,(23)(24)(25). In addition, this peptide is dipsogenic when administered into the central nervous system of rat (26) and stimulates aldosterone secretion from the adrenal cortex (27,28).…”

Section: Discussionmentioning

confidence: 99%

A human neutrophil-dependent pathway for generation of angiotensin II. Purification of the product and identification as angiotensin II.

Wintroub¹,

Klickstein²,

Watt³

1981

J. Clin. Invest.

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A B S T R A C T A human neutrophil lysosomal protease interacts at physiologic pH with a 62,000-67,000-mol wt plasma protein substrate to generate a vasoactive, smooth muscle-contracting "neutral" peptide. The peptide product of this system, previously designated the "neutral" peptide-generating pathway, was generated from purified components and purified by Bio-Gel P2 gel filtration and reverse-phase high performance liquid chromatography with a 50-60% yield of starting activity. The purified peptide had an amino acid composition of Asx, Pro, Val, Ile, Tyr, Phe, His, Arg, a composition identical to that of angiotensin II. The peptide and synthetic angiotensin II each filtered at 48-52% bed volume on Bio-Gel P2, had an isoelectric point of pH 7.8-8.1 at 4°C, migrated 3 cm toward the cathode during pH 6.4 low-voltage paper electrophoresis, and had a retention time of 44.8 min during reverse-phase high-performance liquid chromatography. In addition, the functional activity of the peptide at each purification step correlated with angiotensin II content determined by specific radioimmunoassay. The amino acid sequence of 25 nmol of the peptide was Asp-Arg-Val-Tyr-Ile-His-Pro-Phe, the same covalent structure as that ofangiotensin II. Therefore, under

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Effects of Angiotensin II and Some Analogues on Vascular Permeability in the Rabbit

Cited by 127 publications

References 12 publications

Differences in Mortality Rate between Abrupt and Progressive Carotid Ligation in the Gerbil: Role of Endogenous Angiotensin II

Differences in Mortality Rate between Abrupt and Progressive Carotid Ligation in the Gerbil: Role of Endogenous Angiotensin II

Pulmonary Edema Induced by Angiotensin II in Rats

A human neutrophil-dependent pathway for generation of angiotensin II. Purification of the product and identification as angiotensin II.

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