Obesity and resistant hypertension

Abstract

Obesity is the strongest risk factor for resistance to drug therapy in hypertensive patients, which is caused by a substantial number of pathophysiological mechanisms. One of them is dysregulation of adipokines – peptides produced by a fat tissue; adiponectin is one of them, today it attracts the most attention. Another pathological pathway of development of refractoriness to hypotensive drugs is impairment in regulation between renin-angiotensin-aldosterone (RAAS) and natriuretic peptide (NP) systems, especially in patients with visceral obesity. Pharmacological enhancement NP actions may cause an additive benefit to effects of the RAAS inhibition. Currently ARNI, a novel drug combination of valsartan (angiotensin II receptor inhibitor) and sacubitril (inhibitor of neutral endopeptidase neprilysin, that catalysis the intracellular degradation of NP) is widely discussed in scientific society. Another component of RAAS – aldosterone also plays an important role in development of resistant hypertension in obese people: it has been shown that hyperaldosteronism is a strong risk factor of metabolic syndrome and refractoriness to hypotensive drugs. Further, it is well known, that chronic hyperactivation of sympathetic nervous system often occurs in obese patients with resistant hypertension. The novel non-pharmacological method of renal denervation and a bunch of SYMPLISITY HTN trials will be briefly reviewed. In conclusion specific features of pharmacological treatment of hypertension in obese people, possible side effects of antihypertensive drugs that may affect overweighed patients will be discussed, as well as an impact of weight-reducing drugs in people with hypertension.