Table 2.
Effects on inflammatory cytokines Antihypertensive mechanisms Proposed References | |||
---|---|---|---|
Statins | ↓ IL-1β | NF-κB inhibition AT1R downregulation HMC CoA inhibition (G protein coupled signalling inhibition) PPAR-γ inhibition Upregulates NO synthase |
[162, 164, 166, 167, 174] |
↓ IL-6 | |||
↓ MCP-1 | |||
↓ ICAM-1 | |||
↓ MMP-2 | |||
↓ MMP-9 | |||
↓ hs-CRP | |||
↓ PAI-1 | |||
↑ NO | |||
| |||
ARBs/ACEIs | ↓ IL-1β | NF-κB inhibition AT1R downregulation Decreased ACE synthesis |
[8, 56, 164] |
↓ IL-6 | |||
↑ TGF-β (losartan) | |||
↑ NO (AT2R) | |||
| |||
Calcium channel blockers | ↓ MMP-2 | Protein kinase pathway (MMP-2) | [174, 176] |
↓ MMP-9 | |||
↓ IL-1β | |||
↓ IL-18 | |||
↓ CRP | |||
↓ MCP-1 | |||
↓ ICAM-1 |
IL: interleukin; MCP: macrophage chemotactic factor-1; ICAM-1: intercellular adhesion molecule-1; MMP: matrix metalloproteinase; NO: nitric oxide; ARBs: angiotensinogen receptor blockers; ACEIs: angiotensin converting enzyme inhibitors; NF-κB: nuclear factor κB; AT1R: angiotensinogen type 1 receptor; HMC CoA: hydroxy-methyl-glutaryl coenzyme A; hs-CRP: high sensitivity C reactive protein.