Generalized cerebral vasoconstriction induced by intracarotid infusion of angiotensin II in the rabbit

Reynier-Rebuffel, A. M.; Pinard, Elisabeth; Aubineau, P.; Méric, P.; Seylaz, Jacques

doi:10.1016/0006-8993(83)90965-4

Cited by 14 publications

(3 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Some reports indicate that regionally infused or topically applied AII results in generalized or local cerebral vasoconstriction in rabbits (Reynier-Rebuffel et al, 1983), hamsters (Joyner et al, 1988), and cats (Mayhan et al, 1988;Wei et al, 1978). Conversely, others reported that AII elicits moderate pial vasodilation in the newborn pig (Meng and Busija, 1993), rabbit (Haberl et al, 1991), and rat (Haberl et al, 1990).…”

Section: Discussionmentioning

confidence: 92%

Prostaglandins Contribute to Impaired Angiotensin II–Induced Cerebral Vasodilation after Brain Injury

Baranov

Armstead²

2002

Journal of Neurotrauma

View full text Add to dashboard Cite

This study characterized the effects of fluid percussion brain injury (FPI) on angiotensin II (AII)-induced cerebral vasodilation, determined the role of prostaglandins in such changes and evaluated the contribution of two subtypes of AII receptors (AT(1) and AT(2)) to the effects of AII on cerebrovascular regulation. Topical AII (10(-8), 10(-6), 10(-4) M) elicited vasodilation, which was attenuated by FPI (10 +/- 1; 18 +/- 2; 27 +/- 1% vs. 2 +/- 1; 4 +/- 1; 7 +/- 1%). Such changes in diameter were associated with increases in CSF 6-keto-PGF(1alpha), the stable breakdown product of PGI(2) (1.5 +/- 0.1; 2.1 +/- 0.1; 4.0 +/- 0.3 fold) and TXB(2), the stable breakdown product of TXA(2) (1.2 +/- 0.1; 1.4 +/- 0.1; 1.6 +/- 0.1 fold). However, after FPI, increases in 6-keto PGF(1alpha) were blocked (1.0 +/- 0.1; 1.0 +/- 0.1; 1.1 +/- 0.1 fold) whereas TXB(2) release was enhanced (1.5 +/- 0.1; 1.8 +/- 0.1; 1.9 +/- 0.1 fold). Pretreatment with the cyclooxygenase inhibitor indomethacin (5 mg/kg i.v.) in FPI animals partially protected AII vasodilation (8 +/- 1; 14 +/- 2; 19 +/- 3%). CGP 42112A, a putative AT(2) agonist, elicited vasodilation, which was also blunted by FPI. Such dilation was not associated with CSF prostaglandin changes, and indomethacin did not protect responses altered by FPI. Vasodilatation caused by low concentrations of AII was blunted by an AT(1) antagonist ZD 7155 but unchanged by an AT(2) antagonist PD 123,319. The high AII concentration produced dilation that was blunted by both antagonists. These data show that FPI impairs AII-mediated vasodilation. These data suggest that FPI causes these changes via alteration in an AT(1)-mediated production of prostaglandins. These data additionally suggest that FPI induced impairment of AT(2) mediated vasodilation is independent of an altered production of prostaglandins.

show abstract

Section: Discussionmentioning

confidence: 92%

Prostaglandins Contribute to Impaired Angiotensin II–Induced Cerebral Vasodilation after Brain Injury

Baranov

Armstead²

2002

Journal of Neurotrauma

View full text Add to dashboard Cite

show abstract

“…Vertebral arterial in- fusions in anesthetized dogs raised CSFp (19), and unilateral carotid arterial infusions of the peptide produced a symmetrical reduction in the cerebral blood flow of anesthetized rabbits (20). Vertebral arterial in- fusions in anesthetized dogs raised CSFp (19), and unilateral carotid arterial infusions of the peptide produced a symmetrical reduction in the cerebral blood flow of anesthetized rabbits (20).…”

Section: Discussionmentioning

confidence: 99%

Resistance to Outflow of Cerebrospinal Fluid after Central Infusions of Angiotensin

Morrow

Keil

Severs

1992

Experimental Biology and Medicine

View full text Add to dashboard Cite

Infusions of artificial cerebrospinal fluid (CSF) into the cerebroventricles of conscious rats can raise CSF pressure (CSFp). This response can be modified by some neuropeptides. One of these, angiotensin, facilitates the rise in CSFp. We measured CSFp in conscious rats with a computerized system and evaluated resistance to CSF outflow during infusion of artificial CSF, with or without angiotensin, from the decay kinetics of superimposed bolus injections. Angiotensin (10 ng/min) raised CSFp (P less than 0.05) compared with solvent, but the resistance to CSF outflow of the two groups was similar (P greater than 0.05). Because CSFp was increased by angiotensin without an increase in the outflow resistance, a change in some volume compartment is likely. Angiotensin may raise CSFp by increasing CSF synthesis; this possibility is supported, since the choroid plexuses contain an intrinsic isorenin-angiotensin system. Alternatively, angiotensin may dilate pial arteries, leading to an increased intracranial blood volume.

show abstract

“…Cette hypothèse est d'ailleurs renforcée par le fait que les variations de la PCCL peuvent modifier l'activité électrique et mécanique des cellules musculaires lisses de l'artère cérébrale isolée (Lusamvuku et coll., 1979). (Aubineau, 1983).…”

Section: Problèmes Posés Par La Théorie Métaboliqueunclassified

Donnees Anatomophysiologiques en Faveur d'UN Role Non Vasomoteur De l'INNERVATION Autonome Des Vaisseaux Cerebraux: - Role Trophique Au Cours Du Developpementet De l'AGE Adulte. - Possibilite d'UNE Intervention Indirecte Par l'INTERMEDIAIRE De Cellules Adventicielles

Δημητριαδου¹

View full text Add to dashboard Cite

noradrénergique pendant la vie adulte 45 4.2.1. Les récepteurs 4.2.2. Réactivité des vaisseaux "in vitro" 4.2.3. Réactivité des vaisseaux "in vivo" 4.2.4. Rôle physiologique du système noradrénergique a/ Rôle dans l'hypertension et l'autorégulation b/ Rôle trophique 48 4.3. Réactivité des vaisseaux cérébraux vis-à-vis du SNS pendant le développement 50 4.4. Possibilités d'interventiorVdu système nerveux cholinergique 52 4.5. Possibilité d'une influence des co-transmetteurs d'origine neuronale présents dans les terminaisons noradrénergiques et cholinergiques 53 4.5.1. Peptides 4.5.2. Serotonine 54 4.6. Les effets possibles de l'innervation sensorielle 55 CONCLUSIONS -OBJECTIFS 57 '. CCA = lommon (aratiti artery, ΚΑ -cumuli (diotiil ai In y, ICA -Intel imi carotid artery, l'CA « pottriiortommiinlctittnRaiieiY.ACA

show abstract

Generalized cerebral vasoconstriction induced by intracarotid infusion of angiotensin II in the rabbit

Cited by 14 publications

References 34 publications

Prostaglandins Contribute to Impaired Angiotensin II–Induced Cerebral Vasodilation after Brain Injury

Prostaglandins Contribute to Impaired Angiotensin II–Induced Cerebral Vasodilation after Brain Injury

Resistance to Outflow of Cerebrospinal Fluid after Central Infusions of Angiotensin

Donnees Anatomophysiologiques en Faveur d'UN Role Non Vasomoteur De l'INNERVATION Autonome Des Vaisseaux Cerebraux: - Role Trophique Au Cours Du Developpementet De l'AGE Adulte. - Possibilite d'UNE Intervention Indirecte Par l'INTERMEDIAIRE De Cellules Adventicielles

Contact Info

Product

Resources

About