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MESENTERIC RESISTANCE AND BRAIN MICROVASCULAR ANGIOTENSIN‐CONVERTING ENZYME IN THE SPONTANEOUSLY HYPERTENSIVE RAT
Author(s) -
Jandeleit Karin,
Perich Rose,
Jackson Bruce,
Johnston Colin I.
Publication year - 1992
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1992.tb00469.x
Subject(s) - endocrinology , medicine , angiotensin iii , radioligand , angiotensin converting enzyme , angiotensin ii , blood pressure , renin–angiotensin system , enzyme , chemistry , mesenteric arteries , spontaneously hypertensive rat , angiotensin ii receptor type 1 , receptor , biochemistry , artery
SUMMARY 1. Angiotensin‐converting enzyme (ACE) concentration was measured in mesenteric and brain microvessels from spontaneously hypertensive rats (SHR) and compared with normotensive controls using a specific radioligand binding assay. 2. Plasma angiotensin‐converting enzyme activity was similar in SHR ( n = 15) and normotensive controls ( n = 21; 58 ± 1 nmol HL/mL per min, vs 64 ± 6 nmol HL/mL per min). 3. There was no significant difference between the mesenteric vascular angiotensin‐converting enzyme radioligand binding site density (B max , fmol/ mg protein) of SHR and normotensive controls (954 ±77 vs 890 ±56, P = 0.5, unpaired Student's t ‐test), despite significant differences in systolic blood pressure (220 ± 8 mmHg vs 120 ± 6 mmHg respectively, P < 0.01) and increased mesenteric wet weight to body weight ratio in the hypertensive rats (0.28 ± 0.02 mg/g, n = 5 vs 0.16 ± 0.02 mg/g, n = 7, P < 0.01). 4. Brain vascular angiotensin‐converting enzyme radioligand binding site density (B max , fmol/ mg protein) was also similar in SHR and normotensive controls (467 ±62, n = 5 vs 497 ± 64, n = 5, P = 0.7, unpaired Student's t ‐test). 5. These results demonstrate that vascular angiotensin‐converting enzyme concentration is not altered in the SHR and that vascular ACE is not increased in this form of vascular hypertrophy or regulated by the blood pressure level.