Non-pharmacological aspects of blood pressure management: what are the data?

Abstract

Hypertension affects 29% of US adults and is a significant risk factor for cardiovascular morbidity and mortality. Epidemiological data support contribution of several dietary and other lifestyle-related factors to the development of high blood pressure (BP). Several clinical trials investigated the efficacy of non-pharmacological interventions and lifestyle modifications to reduce BP. Best evidence from randomized controlled trials supports BP-lowering effects of weight loss, the Dietary Approaches to Stop Hypertension (DASH) diet, and dietary sodium (Na(+)) reduction in those with prehypertension, with more pronounced effects in those with hypertension. In hypertensive participants, the effects on BP of DASH combined with low Na(+) alone or with the addition of weight loss were greater than or equal to those of single-drug therapy. Trials where food was provided to participants were more successful in showing a BP-lowering effect. However, clinical studies with long-term follow-up revealed that lifestyle modifications were difficult to maintain. Findings from controlled trials of increased potassium, calcium, or magnesium intake, or reduction in alcohol intake revealed modest BP-lowering effects and are less conclusive. The reported effects of exercise independent of weight loss on BP are inconsistent.

Figure 1. Illustration of a model of sodium (Na⁺) retention causing hypertension in a state of dietary potassium (K⁺) deficiency, mediated by WNK1

During K⁺ depletion, to maintain K⁺ levels, ROMK is downregulated (by endocytosis of ROMK). This downregulation is mediated by an increase in the ratio of L-WNK1 to KS-WNK1 in the kidney, which decreases renal K⁺ secretion to conserve K⁺, but also enhances renal Na⁺ reabsorption via ENaC and NCC, resulting in Na⁺ retention and hypertension. Adapted from Huang et al. Cl⁻, chloride; ENaC, epithelial sodium channel; Na⁺, sodium; NCC, Na⁺/Cl⁻ cotransporter; ROMK, renal outer medullary potassium channel; WNK1, with no lysine kinase 1; KS-WNK1, kidney-specific WNK1; L-WNK1, long WNK1.