There is a high incidence of hypertension after kidney transplantation, which has been associated with the development of left ventricular hypertrophy, an increased risk for acute rejection, lower graft survival, and increased mortality. The pathogenesis of post-transplant hypertension is multifactorial, and therefore optimum therapy for it is not clearly defined. Historically, use of renin-angiotensin system (RAS) blockade in post-transplant hypertension has been limited given concerns of inducing worsening allograft function. Recent data demonstrated that subjects with post-transplant hypertension can be treated effectively with RAS blockers, and that these agents may offer significant additional benefits beyond blood pressure control. Review of the literature suggests that RAS blockers should be considered as useful agents for treatment of post-transplant hypertension not due to transplant renal artery stenosis.