Background: Guidelines recommend that blood pressure (BP) be measured using upper-arm cuff devices. Wrist cuff devices may be appropriate for use in individuals with very large arm circumferences or in other circumstances that prohibit accurate upper-arm measurements. However, the accuracy of wrist cuff devices has long been questioned. This study aimed to compare the accuracy of upper-arm cuff and wrist cuff devices that have undergone standardized validation testing.
Methods: A systematic review of BP device validation studies was conducted through the MEDLINE, Embase, and Web of Science databases from 1987 up to 2023. Studies that followed a recognised validation protocol in an adult population and compared either upper-arm cuff or wrist cuff devices to manual BP (reference standard) were included. A random-effects meta-analysis was performed to estimate pooled mean BP differences (test minus reference).
Results: 345 eligible validation studies were included, comprising 279 studies for upper-arm cuff, and 66 studies for wrist cuff devices. Systolic BP from automated upper-arm and wrist cuff devices showed similar mean differences to the reference standard [pooled mean differences (95% CI): upper-arm 0.1 mmHg (-0.2; 0.3) and wrist -0.2 mmHg (-0.6; 0.3), p=0.36 for between group difference, I2≈85-86%]. The difference in diastolic BP between upper-arm and wrist cuff devices compared to the reference standard was also small [upper-arm -0.3 mmHg (-0.5; -0.1) and wrist 0.1 mmHg (-0.3; 0.6), p=0.051, I2≈86-89%].
Conclusion: The difference in measured BP between validated upper-arm and wrist cuff devices is minimal. These data provide strong evidence that validated wrist cuff devices provide accurate BP measurements when used in a standardized manner and appear appropriate for use in circumstances when reliable upper-arm cuff measurements cannot be obtained.

Background and Aims: Renal arterial infusion of tempol (RAT) at the onset of Gram-negative sepsis has been reported to prevent the development of sepsis-induced medullary hypoperfusion, hypoxia, and acute kidney injury (AKI). However, the efficacy of tempol at reversing renal microcirculatory abnormalities and functional deficits in established septic AKI is unclear. We aimed to test whether a tempol treatment in established sepsis will reverse medullary hypoxia and AKI.
Methods: Following right unilateral nephrectomy, the left kidney was instrumented with a renal arterial catheter and oxygen sensing fibre-optic probes into the renal medulla. At 23-hours of live Escherichia coli infusion, conscious sheep were fluid resuscitated with Hartmann’s solution (30 ml/kg over 0.5-h). Sheep then received intravenous tempol (IVT; 30 mg/kg/h), RAT (3 mg/kg/h) or vehicle from 24-31 h of sepsis. At 31-h of sepsis, sheep were intravenously administered with antibiotics (1 g ceftriaxone) and monitored over a 48-h recovery period.
Results: Sepsis-induced renal medullary hypoxia was attenuated by RAT (25.1±5.5 to 34.3±4.6 mmHg). This protective effect against renal medullary hypoxia with RAT during sepsis was sustained over the 48-hour recovery period (46.8±6.6 mmHg). In contrast, medullary PO2 in IVT treated sheep was lower during treatment and at the end of the recovery period (27.5±5.2 mmHg) compared with the premorbid baseline levels (49.0±5.2 mmHg). Sepsis-induced increases in plasma creatinine progressively declined as the treatment period progressed in RAT such that at the end of the treatment period, it was – 44.5 ± 6.3% less than 23 h sepsis (P = 0.01). In contrast, IVT treatment did not significantly reduce plasma creatinine levels during the treatment period.
Conclusion: In sheep with established septic AKI, RAT attenuated renal medullary tissue hypoxia and AKI and expedited the recovery of medullary tissue PO2 following antibiotic treatment. These reno-protective effects were not observed when tempol was administered intravenously.

Background and aim: Men typically have higher blood pressure (BP) and develop cardiovascular diseases earlier than women. The kidneys regulate body fluid homeostasis and BP by matching sodium excretion to intake. Evidence indicates marked sex differences in sodium excretion, though the mechanisms are not fully understood. This study examined temporal changes in blood pressure and sodium excretion in response to increased sodium intake in male and female rats.

Methods: Three-month-old Sprague Dawley male and female rats were maintained on a normal salt diet (NSD; 0.26% NaCl) for 7 days or switched after 2 days to a high salt diet (HSD; 5% NaCl) for 5 days. Food and water intake, urine excretion (metabolic cage), and BP (via radiotelemetry) were measured continuously, allowing daily construction of pressure natriuresis curves.

Results: At baseline, females had lower mean arterial pressure (MAP) (111±1 vs 115±2 mm Hg, P=0.02) and excreted more sodium (~37%, P<0.0001) than male rats. On Day 5 of HSD, the increase in MAP was greater in males than females (8±3 vs 2±1 mm Hg, P<0.01). Sodium excretion increased more in females than males from day 1 of HSD. In response to HSD, pressure-natriuresis reached a steady state at day 2 of HSD in females but at day 5 of HSD in males. HSD increased proteinuria more in males than females (+33 vs +9.5 mg/day/kg P<0.01). Urinary nitrate/nitrite excretion decreased earlier (Day 1, P=0.0003) in females than in males (day 3, P=0.009).

Conclusions: Our study demonstrates that females adapt more quickly to increased sodium intake than males. Females also excrete excess sodium with a smaller rise in BP, indicating significant sex differences in sodium regulation, which may be associated with differences in nitric oxide bioavailability. A better understanding of sex differences in kidney sodium transport mechanisms may lead to the development of improved treatments.

Background and Aim: Diabetes is the fastest-growing disease in New Zealand. Most (75%) patients with T2D have high blood pressure (BP), and half of BP patients exhibit high blood glucose (BG) such a condition we call “glucotension”. Glucagon-like peptide type -1 (GLP-1) has an essential role in regulating glucose homeostasis but its efficacy has not fully established in glucotension. Given the recent finding of GLP1R expression in the carotid body and hyperactivity of this organ due to higher sympathetic nerve activity (SNA) in hypertension and diabetes, we have sought to test the hypothesis that GLP1R stimulation will modulate glucotension via reducing SNA.

Methods: First time, we report the novel model of “Glucotension” induced using high-fat diet (HFD) and Streptozotocin-STZ (via Osmotic pump delivery system) in spontaneous hypertensive rats (SHR). GLP1 agonist (Exendin-4) was given (acutely & chronically) and chemoreflex testing, blood glucose, glucose tolerance (GTT), cognitive function, BP, renal SNA were assessed. Measurement of cardiac, respiratory (plethysmography) and renal function (ultrasound) were also studied.

Results: Our results showed Exendin-4 attenuates the chemoreflex evoked SNA response along with BP in HFD+STZ fed conscious SH rats (p<0.05). Post-drug treatment, the SHR+HFD+STZ group showed an improvement in glucose tolerance compared to respective control groups. In chronic treatment with Exendin-4, SH rats fed with HFD only also showed improvement in cognitive functions compared to pre-drug values suggesting that improved contextual memory, indicating improvement in cerebral blood flow. SHR-HFD group showed higher systolic dysfunction compared to all other groups and Exendin-4 paused this acceleration with no further decline in dysfunction (P=0.0018).

Conclusion: A novel model of glucotension showed cardiac dysfunction in SHRs that was ameliorated by treatment with a GLP-1 agonist. We conclude that GLP-1 agonist provides a new way to control glucotension potentially via modulating SNA.