There are several mechanisms that link obesity with hypertension and, as with dia­betes, they involve intricate biochemical pathways, although it is still an evolv­ing area of research. Atherosclerotic plaques in patient’s arteries can impair the baroreflex sensitivity leading to impaired parasympathetic cardiac modulation, as a result of affected arteries becoming stiffer. This therefore leads to the sym­pathetic system dominating arterial resistance thereby inducing hypertension [81]. Furthermore, it appears that free fatty acids (FFAs) are critical to inducing hypertension in obese patients. They inhibit Na + /K + ATPase enzymes leading to greater vascular smooth muscle contraction and resistance. However, they can also have a more direct effect on ion channels causing activation of the smooth muscles and again leading to greater vascular resistance [82]. In the early phases of obesity, there is increased renal tubular reabsorption which causes primary retention. However, this is short lived and compensation through renal vasodila­tion and increased glomerular filtration rate tends to normalise the blood pressure. However, incomplete compensation can result in expansion of the extracellu­lar fluid and, over time, resetting of the kidney-fluid balance. This can be aided by compression of the renal medulla causing compression of the vasa recta and loop of Henle [83, 84]. However, the process causing hypertension is much more complex and research suggests hormones such as insulin and leptin, as well as endothelial dysfunction that can result from the pro-inflammatory state in obe­sity all have a role in causing hypertension [85–87]. The reduction in the level of adipocytes following SG would diminish these effects and over 80% of patients reportedly see lasting improvements to their blood pressure [6].