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Calcium channel blockades exhibit anti-inflammatory and antioxidative effects by augmentation of endothelial nitric oxide synthase and the inhibition of angiotensin converting enzyme in the N(G)-nitro-L-arginine methyl ester-induced hypertensive rat aorta: vasoprotective effects beyond the blood pressure-lowering effects of amlodipine and manidipine.
Hypertens Res. 2005 Aug; 28(8):689-700.HR

Abstract

Long-acting dihydropyridine calcium channel blockades have been shown to limit the progression of atherosclerosis and decrease the incidence of cardiovascular events in humans and animals. To investigate the vasoprotective effects beyond the blood pressure-lowering effects of these agents, amlodipine (20 mg/kg/ day) and manidipine (10 mg/kg/day) were administered by gavage to N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats for 2 weeks. L-NAME treatment (0.7 mg/ml in drinking water) significantly decreased the gene and protein expression of endothelial nitric oxide synthase (eNOS) and increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1) mRNA levels in the aorta, as determined by Western blotting and reverse transcription (RT)-polymerase chain reaction (PCR). Amlodipine and manidipine normalized the decreased expression of eNOS gene and protein, and attenuated the overexpression of NADPH oxidase, VCAM-1, and MCP-1 mRNA. Furthermore, amlodipine and manidipine prevented the L-NAME-induced increase in the angiotensin converting enzyme (ACE) mRNA content, thereby restoring control levels in the aorta. On the other hand, hydralazine treatment had no such effect in L-NAME treated rats. Furthermore, the increased expression of manganese superoxide dismutase (Mn-SOD) by L-NAME treatment was not affected by amlodipine, manidipine, or hydralazine. We concluded that the direct anti-inflammatory and antioxidative effects of calcium channel blockades in the aorta of rats with L-NAME-induced hypertension were not likely to have been mediated by the blood pressure-lowering action of these agents, but instead these beneficial effects appear to have been mediated by an augmentation of eNOS expression and by the inhibition of the expression of ACE.

Authors+Show Affiliations

Department of Clinical Pharmacology, Kyoto Pharmaceutical University, Kyoto, Japan. toba@mb.kyoto-phu.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16392774

Citation

Toba, Hiroe, et al. "Calcium Channel Blockades Exhibit Anti-inflammatory and Antioxidative Effects By Augmentation of Endothelial Nitric Oxide Synthase and the Inhibition of Angiotensin Converting Enzyme in the N(G)-nitro-L-arginine Methyl Ester-induced Hypertensive Rat Aorta: Vasoprotective Effects Beyond the Blood Pressure-lowering Effects of Amlodipine and Manidipine." Hypertension Research : Official Journal of the Japanese Society of Hypertension, vol. 28, no. 8, 2005, pp. 689-700.
Toba H, Nakagawa Y, Miki S, et al. Calcium channel blockades exhibit anti-inflammatory and antioxidative effects by augmentation of endothelial nitric oxide synthase and the inhibition of angiotensin converting enzyme in the N(G)-nitro-L-arginine methyl ester-induced hypertensive rat aorta: vasoprotective effects beyond the blood pressure-lowering effects of amlodipine and manidipine. Hypertens Res. 2005;28(8):689-700.
Toba, H., Nakagawa, Y., Miki, S., Shimizu, T., Yoshimura, A., Inoue, R., Asayama, J., Kobara, M., & Nakata, T. (2005). Calcium channel blockades exhibit anti-inflammatory and antioxidative effects by augmentation of endothelial nitric oxide synthase and the inhibition of angiotensin converting enzyme in the N(G)-nitro-L-arginine methyl ester-induced hypertensive rat aorta: vasoprotective effects beyond the blood pressure-lowering effects of amlodipine and manidipine. Hypertension Research : Official Journal of the Japanese Society of Hypertension, 28(8), 689-700.
Toba H, et al. Calcium Channel Blockades Exhibit Anti-inflammatory and Antioxidative Effects By Augmentation of Endothelial Nitric Oxide Synthase and the Inhibition of Angiotensin Converting Enzyme in the N(G)-nitro-L-arginine Methyl Ester-induced Hypertensive Rat Aorta: Vasoprotective Effects Beyond the Blood Pressure-lowering Effects of Amlodipine and Manidipine. Hypertens Res. 2005;28(8):689-700. PubMed PMID: 16392774.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Calcium channel blockades exhibit anti-inflammatory and antioxidative effects by augmentation of endothelial nitric oxide synthase and the inhibition of angiotensin converting enzyme in the N(G)-nitro-L-arginine methyl ester-induced hypertensive rat aorta: vasoprotective effects beyond the blood pressure-lowering effects of amlodipine and manidipine. AU - Toba,Hiroe, AU - Nakagawa,Yoshitsugu, AU - Miki,Shunsuke, AU - Shimizu,Takahiro, AU - Yoshimura,Akiko, AU - Inoue,Riyako, AU - Asayama,Jun, AU - Kobara,Miyuki, AU - Nakata,Tetsuo, PY - 2006/1/6/pubmed PY - 2006/2/1/medline PY - 2006/1/6/entrez SP - 689 EP - 700 JF - Hypertension research : official journal of the Japanese Society of Hypertension JO - Hypertens Res VL - 28 IS - 8 N2 - Long-acting dihydropyridine calcium channel blockades have been shown to limit the progression of atherosclerosis and decrease the incidence of cardiovascular events in humans and animals. To investigate the vasoprotective effects beyond the blood pressure-lowering effects of these agents, amlodipine (20 mg/kg/ day) and manidipine (10 mg/kg/day) were administered by gavage to N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats for 2 weeks. L-NAME treatment (0.7 mg/ml in drinking water) significantly decreased the gene and protein expression of endothelial nitric oxide synthase (eNOS) and increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, vascular cell adhesion molecule-1 (VCAM-1), and monocyte chemoattractant protein-1 (MCP-1) mRNA levels in the aorta, as determined by Western blotting and reverse transcription (RT)-polymerase chain reaction (PCR). Amlodipine and manidipine normalized the decreased expression of eNOS gene and protein, and attenuated the overexpression of NADPH oxidase, VCAM-1, and MCP-1 mRNA. Furthermore, amlodipine and manidipine prevented the L-NAME-induced increase in the angiotensin converting enzyme (ACE) mRNA content, thereby restoring control levels in the aorta. On the other hand, hydralazine treatment had no such effect in L-NAME treated rats. Furthermore, the increased expression of manganese superoxide dismutase (Mn-SOD) by L-NAME treatment was not affected by amlodipine, manidipine, or hydralazine. We concluded that the direct anti-inflammatory and antioxidative effects of calcium channel blockades in the aorta of rats with L-NAME-induced hypertension were not likely to have been mediated by the blood pressure-lowering action of these agents, but instead these beneficial effects appear to have been mediated by an augmentation of eNOS expression and by the inhibition of the expression of ACE. SN - 0916-9636 UR - https://www.unboundmedicine.com/medline/citation/16392774/Calcium_channel_blockades_exhibit_anti_inflammatory_and_antioxidative_effects_by_augmentation_of_endothelial_nitric_oxide_synthase_and_the_inhibition_of_angiotensin_converting_enzyme_in_the_N_G__nitro_L_arginine_methyl_ester_induced_hypertensive_rat_aorta:_vasoprotective_effects_beyond_the_blood_pressure_lowering_effects_of_amlodipine_and_manidipine_ L2 - https://medlineplus.gov/highbloodpressure.html DB - PRIME DP - Unbound Medicine ER -