title: Differential effect of telmisartan and amlodipine on monocyte chemoattractant protein-1 and peroxisome proliferator-activated receptor-gamma gene expression in peripheral monocytes in patients with essential hypertension.
abstract: Monocyte chemoattractant protein-1 (MCP-1) and peroxisome proliferator-activated receptor-γ (PPAR-γ) play a significant role in monocyte activation, vascular inflammation, and atherogenesis. Angiotensin receptor blockers and calcium channel blockers are antihypertensive drugs with established efficacy and a favorable safety profile. We investigated the effect of telmisartan--an angiotensin receptor blocker with PPAR-γ agonist activity--and amlodipine on the activation state of peripheral blood monocytes with respect to MCP-1 and PPAR-γ gene expression in hypertensives. We recruited 31 previously untreated patients with essential hypertension who were randomly assigned to receive treatment with telmisartan (n = 16) or amlodipine (n = 15). Blood samples were taken before and 3 months after therapy initiation. Mononuclear cells were isolated and mRNAs of MCP-1 and PPAR-γ were estimated by real-time quantitative reverse transcription-polymerase chain reaction each time. The 2 treatments decreased all blood pressure components significantly (p <0.001). In contrast, in the amlodipine group, MCP-1 gene expression was significantly downregulated after treatment with telmisartan (from 21.4 ± 20.5 to 8.1 ± 6.5, p = 0.009), whereas the amlodipine group did not show any significant change (12.5 ± 8.5 vs 17.6 ± 16.4, p = NS). In addition, PPAR-γ mRNA levels showed a significant increase in telmisartan-treated patients (from 20 ± 18.5 to 42.6 ± 36, p = 0.006) and no significant alterations in the amlodipine group (from 29.6 ± 42.5 to 24.2 ± 27.7, p = NS). In conclusion, treatment with telmisartan results in a significant attenuation of MCP-1 gene expression and an increase of PPAR-γ gene expression in peripheral monocytes in patients with essential hypertension. Our findings may provide new insights into the cardiovascular protection of telmisartan in hypertensives.
authors.affiliation: Cardiology Department, Heraklion University Hospital, Crete, Greece.
authors.forename: Maria E
authors.initials: ME
authors.lastname: Marketou
authors.forename: Joanna E
authors.initials: JE
authors.lastname: Kontaraki
authors.forename: Nikolaos A
authors.initials: NA
authors.lastname: Tsakountakis
authors.forename: Evangelos A
authors.initials: EA
authors.lastname: Zacharis
authors.forename: George E
authors.initials: GE
authors.lastname: Kochiadakis
authors.forename: Dimitris A
authors.initials: DA
authors.lastname: Arfanakis
authors.forename: Frangiskos
authors.initials: F
authors.lastname: Parthenakis
authors.forename: Gregory
authors.initials: G
authors.lastname: Chlouverakis
authors.forename: Panos E
authors.initials: PE
authors.lastname: Vardas
mesh_terms: D017311:Amlodipine / Q000494:pharmacology* / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001562:Benzimidazoles / Q000494:pharmacology* / Q000627:therapeutic use; D001565:Benzoates / Q000494:pharmacology* / Q000627:therapeutic use; D018932:Chemokine CCL2 / Q000187:drug effects / Q000235:genetics*; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects*; D047495:PPAR gamma / Q000235:genetics*; D012720:Severity of Illness Index; D000077333:Telmisartan
chemical_list: D000959:Antihypertensive Agents; D001562:Benzimidazoles; D001565:Benzoates; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D047495:PPAR gamma; D017311:Amlodipine; D000077333:Telmisartan