TY - JOUR
T1 - Brain kinins are responsible for the pressor effect of intracerebroventricular captopril in spontaneously hypertensive rats
AU - Madeddu, Paolo
AU - Glorioso, Nicola
AU - Soro, Aldo
AU - Tonolo, Giancarlo
AU - Manunta, Paolo
AU - Troffa, Chiara
AU - Demontis, Maria Piera
AU - Varoni, Maria Vittoria
AU - Anania, Vittorio
PY - 1990/4
Y1 - 1990/4
N2 - The role of the brain kallikrein-kinin system in the regulation of arterial blood pressure of normotensive and spontaneously hypertensive rats was evaluated. Intracerebroventricular administration of the kinin antagonist [DArg0]Hyp3-Thi5,8[DPhe7]bradykinin caused no change in mean blood pressure in Wistar-Kyoto, Sprague-Dawley, or spontaneously hypertensive rats. The antagonist proved to be very potent in blocking the pressor effect of intracerebroventricular bradykinin (32±3 vs. 3±1 mm Hg,p2, 48±3 vs. 47±8 mm Hg; norepinephrine, 17±2 vs. 18±2 mm Hg; leucine-enkephaline, 15±2 vs. 16±1 mm Hg; neurotensin, 18±2 vs. 19±1 mm Hg; substance P, 19±2 vs. 19±2 mm Hg). Intracerebroventricular administration of 1 mg captopril, an inhibitor of kininase II (one of the enzymes responsible for kinin degradation), caused no change in mean blood pressure in normotensive rats, whereas it increased mean blood pressure by 44±9 mm Hg (p
AB - The role of the brain kallikrein-kinin system in the regulation of arterial blood pressure of normotensive and spontaneously hypertensive rats was evaluated. Intracerebroventricular administration of the kinin antagonist [DArg0]Hyp3-Thi5,8[DPhe7]bradykinin caused no change in mean blood pressure in Wistar-Kyoto, Sprague-Dawley, or spontaneously hypertensive rats. The antagonist proved to be very potent in blocking the pressor effect of intracerebroventricular bradykinin (32±3 vs. 3±1 mm Hg,p2, 48±3 vs. 47±8 mm Hg; norepinephrine, 17±2 vs. 18±2 mm Hg; leucine-enkephaline, 15±2 vs. 16±1 mm Hg; neurotensin, 18±2 vs. 19±1 mm Hg; substance P, 19±2 vs. 19±2 mm Hg). Intracerebroventricular administration of 1 mg captopril, an inhibitor of kininase II (one of the enzymes responsible for kinin degradation), caused no change in mean blood pressure in normotensive rats, whereas it increased mean blood pressure by 44±9 mm Hg (p
KW - Captopril
KW - Central nervous system
KW - Kallikrein-kinin system
KW - Kinin antagonist
KW - Renin-angiotensin system
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M3 - Article
C2 - 2180818
AN - SCOPUS:0025215516
VL - 15
SP - 407
EP - 412
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 4
ER -