Table 3.
Relevant mechanisms of hypertension after liver transplantation induced by common immunosuppressive agents[42]
| Category | Drug | Mechanism | |
| CNI | TAC, CsA | Increasing vascular tension: reducing nitric oxide (NO) and increasing endothelin level | |
| Increasing sympathetic excitability | |||
| Activating the angiotensin-aldosterone system: elevated blood pressure, water, and sodium retention | |||
| Activating sodium-chloride synergistic transport receptors in distal tubules: increased sodium reabsorption and excessive capacity | |||
| Nephrotoxicity: AKI induced by vasoconstriction Chronic ischemia, glomerulosclerosis, interstitial fibrosis, and tubular atrophy | |||
| Glucocorticoid | Methylprednisolone | Increasing sympathetic excitability | |
| Increasing vascular tension | |||
| Increasing activity of mineralocorticoids | |||
CNI: Calcineurin inhibitor; TAC: Tacrolimus; AKI: Acute kidney injury; CsA: Cyclosporine A.