Role of adrenergic structures in functional control over the cerebral circulation

1978 ◽  
Vol 9 (3) ◽  
pp. 262-265
Author(s):  
S. A. Bugaev
Keyword(s):  
Cerebral Circulation ◽  
Adrenergic Structures ◽  
Functional Control

scholarly journals The role of intramolecular interactions in the functional control of multiheme cytochromesc

FEBS Letters ◽  
2011 ◽  
Vol 586 (5) ◽  
pp. 504-509 ◽  
Author(s):  
Bruno M. Fonseca ◽  
Catarina M. Paquete ◽  
Carlos A. Salgueiro ◽  
Ricardo O. Louro
Keyword(s):  
Intramolecular Interactions ◽  
Functional Control

scholarly journals Corrigendum to “The role of intramolecular interactions in the functional control of multiheme cytochromesc” [FEBS Lett. 586 (2012) 504-509]

FEBS Letters ◽  
2012 ◽  
Vol 586 (19) ◽  
pp. 3536-3536
Author(s):  
Bruno M. Fonseca ◽  
Catarina M. Paquete ◽  
Carlos A. Salgueiro ◽  
Ricardo O. Louro
Keyword(s):  
Intramolecular Interactions ◽  
Functional Control

Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels

1998 ◽  
Vol 78 (1) ◽  
pp. 53-97 ◽  
Author(s):  
FRANK M. FARACI ◽  
DONALD D. HEISTAD
Keyword(s):  
Potassium Channels ◽  
Cerebral Circulation ◽  
Second Messengers ◽  
Chronic Hypertension ◽  
Major Mechanism ◽  
Disease States ◽  
Vasoactive Factors ◽  
New Concepts ◽  
Intracellular Second Messengers

Faraci, Frank M., and Donald D. Heistad. Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels. Physiol. Rev. 78: 53–97, 1998. — Several new concepts have emerged in relation to mechanisms that contribute to regulation of the cerebral circulation. This review focuses on some physiological mechanisms of cerebral vasodilatation and alteration of these mechanisms by disease states. One mechanism involves release of vasoactive factors by the endothelium that affect underlying vascular muscle. These factors include endothelium-derived relaxing factor (nitric oxide), prostacyclin, and endothelium-derived hyperpolarizing factor(s). The normal vasodilator influence of endothelium is impaired by some disease states. Under pathophysiological conditions, endothelium may produce potent contracting factors such as endothelin. Another major mechanism of regulation of cerebral vascular tone relates to potassium channels. Activation of potassium channels appears to mediate relaxation of cerebral vessels to diverse stimuli including receptor-mediated agonists, intracellular second messengers, and hypoxia. Endothelial- and potassium channel-based mechanisms are related because several endothelium-derived factors produce relaxation by activation of potassium channels. The influence of potassium channels may be altered by disease states including chronic hypertension, subarachnoid hemorrhage, and diabetes.

Role of NO in goat basal cerebral circulation and after vasodilatation to hypercapnia or brief ischemias

1993 ◽  
Vol 265 (6) ◽  
pp. R1410-R1415 ◽  
Author(s):  
G. Dieguez ◽  
J. L. Garcia ◽  
N. Fernandez ◽  
A. L. Garcia-Villalon ◽  
L. Monge ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Methyl Ester ◽  
Cerebral Circulation ◽  
Systemic Arterial Pressure ◽  
Nitric Oxide Production ◽  
Hemodynamic Effects ◽  
Arterial Pco2 ◽  
Different Levels

The role of nitric oxide (NO) in the cerebral circulation under basal conditions and after vasodilatation to hypercapnia or reactive hyperemias was studied in 17 anesthetized goats. The intravenous administration of NG-nitro-L-arginine methyl ester (L-NAME, 3-4 or 8-10 mg/kg), an inhibitor of nitric oxide production, reduced middle cerebral artery (MCA) flow (electromagnetically measured) by 19 and 30% and increased systemic arterial pressure by 21 and 26%, respectively, whereas heart rate did not significantly change; MCA resistance increased by 48 and 86%, respectively. These hemodynamic effects were reversed by L-arginine (200-300 mg/kg iv; 5 goats). Different levels of hypercapnia (PCO2 of 30-35, 40-45, and 55-65 mmHg) (12 goats) produced arterial PCO2-dependent increases in MCA flow that were similar under control and L-NAME treatment. Graded cerebral hyperemia occurred after 5, 10, and 20 s of MCA occlusion in 5 goats, but its magnitude was decreased during L-NAME treatment. It suggests that, in the cerebral circulation, nitric oxide 1) produces a basal vasodilator tone and 2) is probably not involved in the vasodilatation to hypercapnia but may mediate hyperemic responses after short brain ischemias.

Role of Autonomic Nervous System in Autoregulation of Human Cerebral Circulation

1971 ◽  
Vol 6 (1-6) ◽  
pp. 203-207 ◽  
Author(s):  
F. Gotoh ◽  
S.-I. Ebihara ◽  
M. Toyoda ◽  
Y. Shinohara
Keyword(s):  
Nervous System ◽  
Autonomic Nervous System ◽  
Cerebral Circulation ◽  
Autonomic Nervous

Compensatory role of NO in cerebral circulation of piglets chronically treated with indomethacin

2002 ◽  
Vol 282 (2) ◽  
pp. R400-R410 ◽  
Author(s):  
Yifan Zhang ◽  
C. W. Leffler
Keyword(s):  
Nitric Oxide ◽  
Cerebrospinal Fluid ◽  
Methyl Ester ◽  
Cerebral Circulation ◽  
No Synthase ◽  
Inhibitory Effects ◽  
Circulatory Control ◽  
Pial Arterioles ◽  
Indomethacin Treatment

We hypothesize that inhibitory effects exist between prostanoids and nitric oxide (NO) in their contributions to cerebral circulation. Piglets (1–4 days old) were divided into three chronically treated (6–8 days) groups: control piglets, piglets treated with indomethacin (75 mg/day), and piglets treated with N ω-nitro-l-arginine methyl ester (l-NAME, 100 mg · kg−1 · day−1). Pial arterioles dilated in response to hypercapnia similarly among the three groups (41 ± 4, 40 ± 6, and 45 ± 11%). Cerebrospinal fluid cAMP increased in control piglets, while cGMP increased in indomethacin-treated piglets. l-NAME, but not 7-nitroindazole, inhibited the response to hypercapnia only in indomethacin-treated piglets (40 ± 6 vs. 17 ± 5%). Topical sodium nitroprusside or iloprost restored dilation in response to hypercapnia. Similar results were obtained when the dilator was bradykinin. Pial arterioles of control and l-NAME-treated piglets constricted in response to ACh (−24 ± 3%). However, those of indomethacin-treated piglets dilated in response to ACh (15 ± 2%). This dilation was inhibited by l-NAME. NO synthase activity, but not endothelial NO synthase expression, increased after chronic indomethacin treatment. These data suggest that chronic inhibition of cyclooxygenase can increase the contribution of NO to cerebrovascular circulatory control in piglets.

scholarly journals Maintenance of cerebral circulation during hemorrhagic hypotension in newborn pigs: role of prostanoids.

1986 ◽  
Vol 59 (5) ◽  
pp. 562-567 ◽  
Author(s):  
C W Leffler ◽  
D W Busija ◽  
D G Beasley ◽  
A M Fletcher
Keyword(s):  
Cerebral Circulation ◽  
Hemorrhagic Hypotension ◽  
Newborn Pigs
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