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Hypertension and diabetes mellitus occur together frequently. There is general consensus in the literature that in patients with hypertension and diabetes, the heart and kidneys are locked in a vice, between arterial stiffening and damage to the microcirculation, with each condition feeding the other in a vicious cycle of events. Decreased glucose tolerance is associated with increased thickness and stiffness of large blood vessels, which contributes to increased blood pressure, macrovascular complications and impaired renal function. Large artery stiffness causes damage to the microvasculature, which in turn increases both capillary rarefaction, initially generated by hypertension and diabetes, and wave reflection. Systolic and pulse pressure are consequently increased, which results in completion of the cycle with more microvascular damage. In addition, macro and microvascular damage appears to increase blood pressure and impair tissue perfusion to target organs, and alterations to the vascular structure of peripheral microvessels in hypertension are related to the impairment of coronary vasodilator capacity. These mechanisms are supported by a large body of data from studies investigating the effects of diabetes and hypertension on the morphology and function of the microvasculature, some of which appear to occur in impaired glucose metabolism, preceding the development of full-blown diabetes. These changes also have important prognostic value, with direct correlations between coronary artery vasoconstriction and the incidence of cardiovascular events. Interventions to break the cycle of events are available, and regimens containing angiotensin-converting enzyme inhibitors have demonstrated good efficacy in increasing coronary reserve. Some of the mechanisms appear to be centred around the inhibition of bradykinin degradation rather than an effect on the renin–angiotensin–aldosterone system.