Mechanisms of FK 506–Induced Hypertension in the Rat

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Mechanisms of FK 506–Induced Hypertension in the Rat by Yoshiyu Takeda, Isamu Miyamori, Kenji Furukawa, Satoru Inaba, and Hiroshi Mabuchi Hypertension Volume 33(1):130-136 January 1, 1999 Copyright © American Heart Association, Inc. All rights reserved.

Systolic blood pressure of 30 rats treated with 0 Systolic blood pressure of 30 rats treated with 0.5 mg · kg−1 · d−1 of FK 506, 30 rats treated with FK 506 (5 mg · kg−1 · d−1), 30 FR 139317–treated rats (FR), 30 FK 506 (5 mg · kg−1 · d−1) plus FR 139317–treated rats, and 30 vehicle-treated rats (C). *P<0.05, FK 5 mg+FR vs C or FR; **P<0.01, FK 5 mg vs C, FR, or FK 5 mg+FR. Systolic blood pressure of 30 rats treated with 0.5 mg · kg−1 · d−1 of FK 506, 30 rats treated with FK 506 (5 mg · kg−1 · d−1), 30 FR 139317–treated rats (FR), 30 FK 506 (5 mg · kg−1 · d−1) plus FR 139317–treated rats, and 30 vehicle-treated rats (C). *P<0.05, FK 5 mg+FR vs C or FR; **P<0.01, FK 5 mg vs C, FR, or FK 5 mg+FR. Yoshiyu Takeda et al. Hypertension. 1999;33:130-136 Copyright © American Heart Association, Inc. All rights reserved.

Aortic eNOS activity (top) in FK 506 (0 Aortic eNOS activity (top) in FK 506 (0.5 mg or 5 mg · kg−1 · d−1)–treated rats (n=5), FR 139317–treated rats (FR, n=5), vehicle- treated rats (C, n=5), and FR 139317 plus FK 506 (5 mg · kg−1 · d−1)–treated rats (n=5). Aortic eNOS activity (top) in FK 506 (0.5 mg or 5 mg · kg−1 · d−1)–treated rats (n=5), FR 139317–treated rats (FR, n=5), vehicle- treated rats (C, n=5), and FR 139317 plus FK 506 (5 mg · kg−1 · d−1)–treated rats (n=5). The endothelial cells were collected from the aortae of 3 rats. eNOS activity was assayed following [14C]l-citrulline formation from [14C]l-arginine. Aortic eNOS activity of FK 506–induced hypertensive rats and rats treated with FK 506 and FR 139317 were significantly decreased compared with control rats or FR 139317–treated rats (P<0.05). Middle shows the concentration of ET-1 mRNA, and lower panel shows eNOS mRNA levels in mesenteric arteries of FK 506 (0.5 mg or 5 mg · kg−1 · d−1)–treated rats (n=7), FR 139317–treated rats (FR, n=7), vehicle–treated rats (C, n=7), and FR 139317 plus FK 506 (5 mg · kg−1 · d−1)–treated rats (n=7). ET-1 mRNA concentrations in the vasculature of FK 506–induced hypertensive rats and rats treated with FK 506 and FR 139317 were significantly increased compared with control rats or FR 139317–treated rats (P<0.05). Aortic eNOS mRNA concentrations in FK 506–induced hypertensive rats and rats treated with FK 506 and FR 139317 were significantly decreased compared with control rats or FR 139317–treated rats (P<0.05). Yoshiyu Takeda et al. Hypertension. 1999;33:130-136 Copyright © American Heart Association, Inc. All rights reserved.

Effect of concentration of the competitive template on the amplification of PCR products derived from ET-1, ECE-1, and CNP cDNAs of mesenteric arteries or aortic eNOS cDNA and each competitive template (Mimic). Effect of concentration of the competitive template on the amplification of PCR products derived from ET-1, ECE-1, and CNP cDNAs of mesenteric arteries or aortic eNOS cDNA and each competitive template (Mimic). Yoshiyu Takeda et al. Hypertension. 1999;33:130-136 Copyright © American Heart Association, Inc. All rights reserved.