Effects of captopril on cerebral blood flow in normotensive and hypertensive rats
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Effects of captopril on cerebral blood flow in normotensive and hypertensive rats. / Barry, D I; Paulson, O B; Jarden, J O; Juhler, M; Graham, D I; Strandgaard, S.
I: The American Journal of Medicine, Bind 76, Nr. 5B, 31.05.1984, s. 79-85.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Effects of captopril on cerebral blood flow in normotensive and hypertensive rats
AU - Barry, D I
AU - Paulson, O B
AU - Jarden, J O
AU - Juhler, M
AU - Graham, D I
AU - Strandgaard, S
PY - 1984/5/31
Y1 - 1984/5/31
N2 - Cerebrovascular effects of the angiotensin converting enzyme inhibitor captopril were examined in normotensive and hypertensive rats. Cerebral blood flow was measured with the intracarotid 133xenon injection method in halothane-anesthetized animals. The blood-brain barrier permeability of captopril (determined with an integral-uptake method) was negligible, the permeability-surface area product in most brain regions being 1 X 10(-5) cm3/g per second, that is, three to four times lower than that of sodium ion. When administered into the cerebral ventricles to bypass the blood-brain barrier, captopril had no effect on cerebral blood flow: furthermore, cerebral blood flow autoregulation (studied by raising and lowering blood pressure) was identical to that in controls. In contrast, when given intravenously, captopril had a marked effect on cerebral blood flow autoregulation--both the lower and upper limits of autoregulation being shifted to a lower pressure (by about 20 to 30 and 50 to 60 mm Hg, respectively), and the autoregulatory range was shortened by about 40 mm Hg. This effect may be ascribed to inhibition of converting enzyme in the cerebral blood vessels rather than within the brain.
AB - Cerebrovascular effects of the angiotensin converting enzyme inhibitor captopril were examined in normotensive and hypertensive rats. Cerebral blood flow was measured with the intracarotid 133xenon injection method in halothane-anesthetized animals. The blood-brain barrier permeability of captopril (determined with an integral-uptake method) was negligible, the permeability-surface area product in most brain regions being 1 X 10(-5) cm3/g per second, that is, three to four times lower than that of sodium ion. When administered into the cerebral ventricles to bypass the blood-brain barrier, captopril had no effect on cerebral blood flow: furthermore, cerebral blood flow autoregulation (studied by raising and lowering blood pressure) was identical to that in controls. In contrast, when given intravenously, captopril had a marked effect on cerebral blood flow autoregulation--both the lower and upper limits of autoregulation being shifted to a lower pressure (by about 20 to 30 and 50 to 60 mm Hg, respectively), and the autoregulatory range was shortened by about 40 mm Hg. This effect may be ascribed to inhibition of converting enzyme in the cerebral blood vessels rather than within the brain.
KW - Angiotensin-Converting Enzyme Inhibitors
KW - Animals
KW - Autoradiography
KW - Blood Pressure/drug effects
KW - Blood-Brain Barrier/drug effects
KW - Captopril/administration & dosage
KW - Cerebral Arteries/drug effects
KW - Cerebrovascular Circulation/drug effects
KW - Homeostasis/drug effects
KW - Hypertension/drug therapy
KW - Injections, Intravenous
KW - Injections, Intraventricular
KW - Proline/analogs & derivatives
KW - Rats
KW - Rats, Inbred Strains
KW - Xenon Radioisotopes
U2 - 10.1016/0002-9343(84)90890-8
DO - 10.1016/0002-9343(84)90890-8
M3 - Journal article
C2 - 6328989
VL - 76
SP - 79
EP - 85
JO - American Journal of Medicine
JF - American Journal of Medicine
SN - 0002-9343
IS - 5B
ER -
ID: 276120490