Effect of atriopeptin on blood flow to cerebrum and choroid plexus

1989 ◽  
Vol 257 (6) ◽  
pp. R1365-R1369
Author(s):  
K. A. Schalk ◽  
J. L. Williams ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Choroid Plexus ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain ◽  
Increased Blood Flow

The goal of this study was to determine whether atriopeptin alters blood flow to cerebrum and choroid plexus. In anesthetized rabbits, blood flow (microspheres) to cerebrum and choroid plexus under control conditions was 36 +/- 3 (mean +/- SE) and 573 +/- 78 ml.min-1.100 g-1, respectively. Infusion of atriopeptin (75, 225, 1,150 ng.kg-1.min-1 iv) increased blood flow to choroid plexus by 22 +/- 11, 53 +/- 26, and 51 +/- 13%, respectively. In contrast, blood flow to cerebrum was not altered by atriopeptin, presumably because the blood-brain barrier prevented access to cerebral vascular smooth muscle. Because a major role of atriopeptin may be to modulate responses to angiotensin II, we examined effects of atriopeptin on vasoconstrictor responses to angiotensin II in the choroid plexus. Angiotensin II was infused in the presence or absence of atriopeptin (300 ng.kg-1.min-1 iv). Angiotensin II (100 ng.kg-1.min-1 iv) decreased blood flow to choroid plexus by 49 +/- 12% and by 47 +/- 14% during simultaneous infusion of atriopeptin. In summary, atriopeptin 1) increases blood flow to choroid plexus, but not cerebrum, and 2) does not appear to attenuate vasoconstrictor effects of angiotensin II in the choroid plexus.

scholarly journals Altered Blood Brain Barrier Integrity in Hypertensive Rats: Role of Angiotensin II.

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Sook Jin Son ◽  
Sahra Ahmadi ◽  
Jessica A. Filosa ◽  
Javier E. Stern
Keyword(s):  
Angiotensin Ii ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Hypertensive Rats ◽  
Barrier Integrity ◽  
Blood Brain ◽  
Altered Blood ◽  
Blood Brain Barrier Integrity

Heterogeneity of brain blood flow and permeability during acute hypertension

1985 ◽  
Vol 249 (3) ◽  
pp. H629-H637 ◽  
Author(s):  
G. L. Baumbach ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Brain Stem ◽  
Blood Brain Barrier ◽  
Regional Differences ◽  
Severe Hypertension ◽  
Brain Barrier ◽  
Acute Hypertension ◽  
Blood Brain ◽  
The Brain ◽  
Increased Blood Flow

The purpose of this study was to examine regional autoregulation of blood flow in the brain during acute hypertension. In anesthetized cats severe hypertension increased blood flow more in cerebrum (159%) and cerebellum (106%) than brain stem (58%). In contrast to the heterogeneous autoregulatory response, hypocapnia produced uniform vasoconstriction in the brain. We also compared vasodilatation during severe hypertension with vasodilatation during hypercapnia. During hypercapnia, blood flow increased as much in brain stem, as in cerebrum and cerebellum. Thus regional differences in autoregulation appear to be specific for autoregulatory stimulus and are not secondary to nonspecific differences in vasoconstrictor or vasodilator capacity. To determine whether the blood-brain barrier is more susceptible to hypertensive disruption in regions with less effective autoregulation, permeability of the barrier was quantitated with 125I-albumin. Severe hypertension produced disruption of the barrier in cerebrum but not in brain stem. Thus there are parallel differences in effectiveness of autoregulation and susceptibility to disruption of the blood-brain barrier in different regions of the brain.

Abstract 050: Essential Role of Cerebral Endothelial AT1 Receptors in the Blood-Brain Barrier Disruption Induced by Angiotensin-II Hypertension

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Monica M Santisteban ◽  
Sung Ji Ahn ◽  
Diane Lane ◽  
Giuseppe Faraco ◽  
Lidia Garcia-Bonilla ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Blood Brain Barrier ◽  
Essential Role ◽  
Brain Barrier ◽  
At1 Receptors ◽  
Barrier Disruption ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Brain Barrier Disruption

Abstract 137: Vascular Smooth Muscle Cell MYPT1 Deficiency Induces Phenotype Switching and Disrupts Blood-Brain Barrier After Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Lizhen Fan ◽  
Liwen Zhu ◽  
Hailan Meng ◽  
Yun Xu
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Protein Expression ◽  
Blood Brain Barrier ◽  
Proteomic Analysis ◽  
Brain Barrier ◽  
Neurological Deficits ◽  
Blood Brain ◽  
Phenotype Switching ◽  
The Impact

Objectives: Cerebral autoregulation and blood brain barrier (BBB) are often impaired in hypertensive and aging individuals, contributing to the development of stroke. Vascular smooth muscle cells (VSMC) play a vital role in cerebral blood flow control and maintenance of BBB. Ischemic injury triggers VSMC to switch into a detrimental phenotype in peripheral blood vessels, however, the pathological phenotype switching in cerebral VSMC and the impact of VSMC on BBB are not elucidated thoroughly in stroke with hypertension. Methods: Hypertensive mice with smooth muscle–specific deletion of MYPT1 (MYPT1 SMKO mice) were generated. Middle cerebral artery occlusion (MCAO) was conducted in adult MYPT1 SMKO mice and their wild-type (WT) mice for 60 min. Ischemic infarct volumes and neurological function were evaluated. Evens blue, immunofluorescence (IF), western blot (WB) and so on were performed to evaluate the permeability of BBB after stroke. The phenotype switching of VSMC was measured by WB, IF and quantitative real-time polymerase chain reaction (q-PCR) in oxygen glucose deprivation (OGD) and co-cultured in vitro models. Proteomic analysis was performed in cerebral capillaries. The q-PCR and WB were used for further validation. Results: It was found that the infarct volumes and neurological deficits were aggravated in MYPT1 SMKO mice and the permeability of BBB was increased. The loss of pericyte cells and degradation of basement membrane of BBB were more severe in MYPT1 SMKO mice. Furthermore, the protein expression of α-SMA in MYPT1 SMKO mice after MCAO was reduced and the protein expression of Calponin and SM-22α was reduced. The ability of migration and proliferation in VSMC of MYPT1-knockout was altered after OGD. Proteomic analysis showed that the expression of protein associated with inflammation in VSMC of MYPT1 SMKO mice was increased than that of WT mice, but the specific protein underlying the mechanism needs further verification. Conclusions: The damage of BBB was increased in MYPT1 SMKO hypertensive mice. And there is a phenotype switching in cerebral VSMC after stroke in MYPT1 SMKO hypertensive mice. The potential mechanism may involve the increasing expression of protein associated with inflammation in VSMC that needs further verification.

The treatment of brain metastasis from breast cancer, role of blood-brain barrier disruption and early experience with trastuzumab

Therapy ◽  
2006 ◽  
Vol 3 (1) ◽  
pp. 97-112 ◽  
Author(s):  
Rose Marie Tyson ◽  
Dale F Kraemer ◽  
Matthew A Hunt ◽  
Leslie L Muldoon ◽  
Peter Orbay ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Brain Metastasis ◽  
Blood Brain Barrier ◽  
Early Experience ◽  
Brain Barrier ◽  
Barrier Disruption ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Brain Barrier Disruption

Role of Microfluidics in Blood-Brain Barrier Permeability Cell Culture Modeling: Relevance to CNS Disorders

2016 ◽  
Vol 15 (3) ◽  
pp. 301-309 ◽  
Author(s):  
Alexander L. Rusanov ◽  
Natalia G. Luzgina ◽  
George E. Barreto ◽  
Gjumrakch Aliev
Keyword(s):  
Cell Culture ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Cns Disorders ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Evidence that disruption of the blood-brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy.

Hypertension ◽  
1984 ◽  
Vol 6 (2_pt_2) ◽  
Author(s):  
K Tamaki ◽  
S Sadoshima ◽  
G L Baumbach ◽  
C Iadecola ◽  
D J Reis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Brain Barrier ◽  
Hypertensive Encephalopathy ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Plasma and cerebrospinal fluid inflammation and the blood-brain barrier in older surgical patients: the Role of Inflammation after Surgery for Elders (RISE) study

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Sarinnapha M. Vasunilashorn ◽  
◽  
Long H. Ngo ◽  
Simon T. Dillon ◽  
Tamara G. Fong ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Blood Brain Barrier ◽  
Plasma Levels ◽  
Inflammatory Markers ◽  
Brain Barrier ◽  
Markers Of Inflammation ◽  
Blood Brain ◽  
Csf Levels ◽  
The Relationship

Abstract Background Our understanding of the relationship between plasma and cerebrospinal fluid (CSF) remains limited, which poses an obstacle to the identification of blood-based markers of neuroinflammatory disorders. To better understand the relationship between peripheral and central nervous system (CNS) markers of inflammation before and after surgery, we aimed to examine whether surgery compromises the blood-brain barrier (BBB), evaluate postoperative changes in inflammatory markers, and assess the correlations between plasma and CSF levels of inflammation. Methods We examined the Role of Inflammation after Surgery for Elders (RISE) study of adults aged ≥ 65 who underwent elective hip or knee surgery under spinal anesthesia who had plasma and CSF samples collected at baseline and postoperative 1 month (PO1MO) (n = 29). Plasma and CSF levels of three inflammatory markers previously identified as increasing after surgery were measured using enzyme-linked immunosorbent assay: interleukin-6 (IL-6), C-reactive protein (CRP), and chitinase 3-like protein (also known as YKL-40). The integrity of the BBB was computed as the ratio of CSF/plasma albumin levels (Qalb). Mean Qalb and levels of inflammation were compared between baseline and PO1MO. Spearman correlation coefficients were used to determine the correlation between biofluids. Results Mean Qalb did not change between baseline and PO1MO. Mean plasma and CSF levels of CRP and plasma levels of YKL-40 and IL-6 were higher on PO1MO relative to baseline, with a disproportionally higher increase in CRP CSF levels relative to plasma levels (CRP tripled in CSF vs. increased 10% in plasma). Significant plasma-CSF correlations for CRP (baseline r = 0.70 and PO1MO r = 0.89, p < .01 for both) and IL-6 (PO1MO r = 0.48, p < .01) were observed, with higher correlations on PO1MO compared with baseline. Conclusions In this elective surgical sample of older adults, BBB integrity was similar between baseline and PO1MO, plasma-CSF correlations were observed for CRP and IL-6, plasma levels of all three markers (CRP, IL-6, and YKL-40) increased from PREOP to PO1MO, and CSF levels of only CRP increased between the two time points. Our identification of potential promising plasma markers of inflammation in the CNS may facilitate the early identification of patients at greatest risk for neuroinflammation and its associated adverse cognitive outcomes.

Sign in / Sign up

Export Citation Format

Share Document