Objective: The association between high salt intake and blood pressure is well-recognised. In overweight/obese individuals, obesity-associated hyperinsulinaemia augments renal sodium reabsorption and in combination with high salt intake this may… Click to show full abstract
Objective: The association between high salt intake and blood pressure is well-recognised. In overweight/obese individuals, obesity-associated hyperinsulinaemia augments renal sodium reabsorption and in combination with high salt intake this may alter blood pressure and arterial haemodynamics. We determined whether short-term high salt intake altered reservoir-excess pressure and central artery haemodynamic parameters in overweight/obese individuals. Design and method: We studied 15 middle-aged and older adults (59.3 ± 6.4 yrs, 5F) who were overweight/obese with elevated systolic blood pressure (130 < SBP < 159 mmHg). In a double-blind cross-over design, they were randomly assigned to seven days of low salt diet (LSD: 50 mmol/day) or high salt intake (HIS: LSD with 200 mmol/day of sodium tablets) separated by a two-week washout period. The parameters derived from reservoir-excess pressure analysis including reservoir pressure integral, peak reservoir pressure (MAXPR), excess pressure integral (INTXSP), peak excess pressure (MAXXSP), systolic rate constant and diastolic rate constant (DRC) were obtained by radial artery tonometry. Additionally central artery haemodynamic parameters including aortic systolic pressure (aSBP), diastolic pressure (aDBP), pulse pressure (aPP) and subendocardial viability index (SVI) were derived from ensemble-averaged radial pulse waveform using generalised transfer function. Aortic pulse wave velocity (aPWV) was estimated as proposed by Hughes et al (Front Physiol. 2020). Results: MAXPR (111.0 ± 10.9 vs 105.4 ± 10.4 mmHg), MAXXSP (41.7 ± 12.0 vs 36.6 ± 5.7 mmHg) and DRC (2.0 ± 0.4 vs 1.8 ± 0.3 s-1) were higher following HIS compared to LSD (p < 0.05). There was no convincing evidence that INTXSP was greater following HIS than LSD (6.9 ± 3.2 vs 5.8 ± 1.6 mmHg s, p = 0.055). aSBP (126.3 ± 15.4 vs 117.6 ± 10.1 mmHg), aDBP (76.3 ± 6.2 vs 73.1 ± 6.3 mmHg) and aPP (50.0 ± 17.4 vs 44.5 ± 10.8 mmHg) were also higher following HIS compared to LSD (p < 0.05). SVI was similar between HIS and LSD (162.7 ± 29.6 vs 171.6 ± 25.0 %, p = 0.143). A greater aPWV was observed following HIS compared to LSD (5.6 ± 1.6 vs 4.9 ± 0.8 m/s, p = 0.034). Conclusions: Short-term HIS adversely alters reservoir function and central artery haemodynamics in overweight/obese adults. These observations suggest a potential mechanism that may increase cardiovascular disease risk associated with HIS in this population.
               
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