Mediators of target organ damage in hypertension: focus on obesity associated factors and inflammation.
Arterial hypertension represents a major cardiovascular epidemic in the developed and developing world. Projections out to 2025 suggest that up to 50% of the adult populations of Western countries will meet standard guideline definitions of hypertension and thus require therapeutic intervention both non-pharmacological or pharmacological. Hyper-tension is also a component of many other major comorbidities contributing to cardiovascular disease burden. These include obesity, the metabolic syndrome, hyperlipidaemia, diabetes, and chronic kidney disease (CKD). Downstream consequences initially presenting as target organ damage of various degrees include coronary artery disease, cerebrovascular disease, nephropathy and chronic heart failure. Although elevated blood pressure per se is undoubtedly the major factor contributing to hypertensive target organ damage there is clear evidence that other mediators are also crucially involved in the transition from a healthy to a diseased state of target organs in the clinical setting of elevated blood pressure. This has obvious consequences for a multifactorial approach aimed not only at achieving target blood pressure levels but also at preventing the development or the progression of target organ damage in order to optimally reduce the overall cardiovascular risk for patients. The epidemic we are currently facing in regards to obesity is closely associated with the expected increase in the prevalence of hypertension. A closer look into the role of obesity and associated factors for the rise in blood pressure and their role in target organ damage is therefore inevitable. This review will thus focus on the clinically important aspects of target organ damage associated with hypertension, particularly obesity related hypertension, and the evidence for the involvement of neurohormonal activation and inflammatory pathways.
Dawood
T
T
Neurovascular Hypertension and Kidney Disease Laboratory, Baker IDI Heart and Diabetes Institute and Alfred Hospital, Melbourne, Australia.
Schlaich
M P
MP
D000328:Adult; D000419:Albuminuria / Q000175:diagnosis; D002318:Cardiovascular Diseases / Q000453:epidemiology* / Q000517:prevention & control; D015897:Comorbidity; D019049:Developed Countries; D003906:Developing Countries; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000503:physiopathology; D005544:Forecasting; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000235:genetics / Q000473:pathology / Q000503:physiopathology* / Q000628:therapy; D017379:Hypertrophy, Left Ventricular / Q000175:diagnosis / Q000453:epidemiology / Q000503:physiopathology; D007249:Inflammation; D007674:Kidney Diseases / Q000453:epidemiology / Q000473:pathology / Q000503:physiopathology; D018377:Neurotransmitter Agents / Q000627:therapeutic use; D009765:Obesity / Q000150:complications* / Q000453:epidemiology / Q000473:pathology; D015995:Prevalence; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology
D018377:Neurotransmitter Agents