Cerebrovascular aspects of converting-enzyme inhibition II: Blood-brain barrier permeability and effect of intracerebroventricular administration of captopril
Research output: Contribution to journal › Journal article › Research › peer-review
Standard
Cerebrovascular aspects of converting-enzyme inhibition II : Blood-brain barrier permeability and effect of intracerebroventricular administration of captopril. / Jarden, J O; Barry, D I; Juhler, M; Graham, D I; Strandgaard, S; Paulson, O B.
In: Journal of Hypertension, Vol. 2, No. 6, 12.1984, p. 599-604.Research output: Contribution to journal › Journal article › Research › peer-review
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Cerebrovascular aspects of converting-enzyme inhibition II
T2 - Blood-brain barrier permeability and effect of intracerebroventricular administration of captopril
AU - Jarden, J O
AU - Barry, D I
AU - Juhler, M
AU - Graham, D I
AU - Strandgaard, S
AU - Paulson, O B
PY - 1984/12
Y1 - 1984/12
N2 - The blood-brain barrier permeability to captopril, and the cerebrovascular effects of intracerebroventricular administration of captopril, were studied in normotensive Wistar rats. The blood-brain barrier permeability-surface area product (PS), determined by an integral-uptake method, was about 1 X 10(-5) cm3/g/s in all brain regions studied. This was three to four times lower than the simultaneously determined PS of Na+ and Cl-, both of which are known to have very low blood-brain barrier permeability. Cerebral blood flow, determined by the intra-arterial 133xenon injection method, was unaffected by intracerebroventricular administration of 100 micrograms captopril. Furthermore the lower limit of cerebral blood flow autoregulation during haemorrhagic hypotension was also unaffected, being in the mean arterial pressure range (50-69 mmHg) in both controls and captopril-treated rats. It was concluded that the blood-brain barrier permeability of captopril was negligible and that inhibition of the brain renin-angiotensin system has no effect on global cerebral blood flow. The cerebrovascular effects of intravenously administered captopril (a resetting to lower pressure of the limits and range of cerebral blood flow autoregulation) are probably exerted via converting enzyme on the luminal surface of cerebral vessels.
AB - The blood-brain barrier permeability to captopril, and the cerebrovascular effects of intracerebroventricular administration of captopril, were studied in normotensive Wistar rats. The blood-brain barrier permeability-surface area product (PS), determined by an integral-uptake method, was about 1 X 10(-5) cm3/g/s in all brain regions studied. This was three to four times lower than the simultaneously determined PS of Na+ and Cl-, both of which are known to have very low blood-brain barrier permeability. Cerebral blood flow, determined by the intra-arterial 133xenon injection method, was unaffected by intracerebroventricular administration of 100 micrograms captopril. Furthermore the lower limit of cerebral blood flow autoregulation during haemorrhagic hypotension was also unaffected, being in the mean arterial pressure range (50-69 mmHg) in both controls and captopril-treated rats. It was concluded that the blood-brain barrier permeability of captopril was negligible and that inhibition of the brain renin-angiotensin system has no effect on global cerebral blood flow. The cerebrovascular effects of intravenously administered captopril (a resetting to lower pressure of the limits and range of cerebral blood flow autoregulation) are probably exerted via converting enzyme on the luminal surface of cerebral vessels.
KW - Angiotensin-Converting Enzyme Inhibitors
KW - Animals
KW - Autoradiography
KW - Blood Pressure/drug effects
KW - Blood-Brain Barrier
KW - Brain/pathology
KW - Capillary Permeability
KW - Captopril/metabolism
KW - Cerebrovascular Circulation/drug effects
KW - Chlorides/metabolism
KW - Homeostasis
KW - Injections, Intraventricular
KW - Male
KW - Proline/analogs & derivatives
KW - Rats
KW - Rats, Inbred Strains
KW - Sodium/metabolism
U2 - 10.1097/00004872-198412000-00004
DO - 10.1097/00004872-198412000-00004
M3 - Journal article
C2 - 6098609
VL - 2
SP - 599
EP - 604
JO - Journal of Hypertension, Supplement
JF - Journal of Hypertension, Supplement
SN - 0952-1178
IS - 6
ER -
ID: 275995183