Why the study?
Improving blood pressure control and reducing unfavorable cardiovascular and renal outcomes in patients with refractory HTN is an urgent clinical problem.
Sympathetic nervous system overactivity is a key pathogenetic factor in refractory hypertension, highlighting the potential therapeutic utility of SGLT2 inhibitors, reserpine, and firibastat.
Answers are grounded in this paper and cite their sources.
Higher SNS activity in refractory HTN on chlorthalidone plus MRA; leaves open sympathetic modulation as adjunctive strategy.
Improving blood pressure (BP) control and reducing the risk of developing unfavorable cardiovascular and renal outcomes in patients with refractory hypertension (HTN) is an urgent problem of cardiology. According to clinical studies, patients with refractory HTN receiving intensive diuretic therapy with chlorthalidone and a mineralcorticoid receptor antagonist differ from patients with refractory HTN by a higher sympathetic nervous system (SNS) activity. Overactivity of sympathetic nerves may be one of the key pathogenetic factors that is involved in the kidney in the formation of refractory HTN, exerting a direct stimulating effect on the type 3 Na+ / H+ exchanger (NHE3) and type 2 sodium glucose cotransporter (SGLT2), which are involved in BP control by mechanism of pressure natriuresis. The review presents data on the peculiarities of sympathetic regulation of sodium tubular transport and the results of studies devoted the elucidating in the patients with resistant and refractory HTN the clinical efficacy of SGLT2 inhibitors glyflozins, sympatholytic reserpine and brain aminopeptidase A inhibitor firibastat, which suppresses the activity of central structures of SNS.
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Ob et al. (2022) studied this question.
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