Hypertension Research最新文献

The synergistic interplay between cortisol and aldosterone is critical for maintaining homeostasis, particularly in blood pressure regulation, fluid balance, and stress response. Cortisol, a glucocorticoid, and aldosterone, a mineralocorticoid, often act in tandem to regulate sodium retention and blood volume. Dysregulation of these hormones, as seen in hyperaldosteronism or Cushing's syndrome, contributes to hypertension and metabolic imbalances. The synergistic effects of autonomous cortisol secretion (ACS) and aldosterone on vascular calcification, focusing on patients with primary aldosteronism (PA). Update findings reveal that cortisol and aldosterone synergistically promote vascular calcification via mineralocorticoid receptor (MR)-dependent pathways, a mechanism effectively attenuated by MR antagonism. Despite a relatively small ACS subgroup, the study highlights critical insights into the cardiovascular risks associated with ACS and PA, emphasizing the need for larger, multicenter studies and long-term outcome data. We might underscore the potential of MR antagonists in mitigating cardiovascular risks and pave the way for broader applications to other conditions involving cortisol dysregulation, such as adrenal incidentalomas and subclinical Cushing's syndrome.

Excessive fructose intake causes a variety of adverse conditions (e.g., obesity, hepatic steatosis, insulin resistance and uric acid overproduction). High fructose-induced hypertension is a particularly common and pathologically significant condition induced by excess fructose, but its underlying mechanisms remain unknown. We investigated these mechanisms in 7-week-old male Sprague-Dawley rats fed normal rat food or a diet containing 60% glucose (GLU group) or 60% fructose (FRU group) for 3, 6, or 12 weeks. Daily food consumption was measured to avoid between-group discrepancies in caloric/salt intake, adjusting for feeding amounts. The mean blood pressure of FRU rats was significantly higher (12 weeks GLU: 94.8 ± 3.4 mmHg vs. 12 weeks FRU: 103.7 ± 1.2 mmHg), and fractional sodium excretion was significantly lower (12 weeks GLU: 0.084 ± 0.011% vs. 12 weeks FRU: 0.059 ± 0.08%), indicating that the high-fructose diet caused salt retention. The kidney weight and glomerular surface area were greater in FRU rats (12 weeks GLU: 7495 ± 181 vs. 12 weeks FRU: 9831 ± 164 μm²), suggesting that the high-fructose diet induced an increase in extracellular fluid volume. The expressions of GLUT5 and ketohexokinase, an enzyme required for fructose metabolism, were up-regulated in the FRU group rats (GLUT5 12 weeks GLU: 104.7 ± 15.4% vs. 12 weeks FLU: 309.0 ± 99.9%, ketohexokinase 12 weeks GLU: 129.6 ± 3.5% vs. 12 weeks FLU: 163.9 ± 13.0%). Cortical ATP levels were significantly lower in FRU rats (12 weeks GLU: 9.82 ± 1.26 nmol/mg protein vs. 12 weeks FRU: 7.59 ± 1.68 nmol/mg protein), possibly indicating ATP consumption due to fructose metabolism. Unlike in previous reports the high-fructose diet did not affect NHE3 expression (12 weeks GLU: 166.1 ± 6.3% vs. 12 weeks FLU: 142.0 ± 5.9%). A gene chip analysis conducted to identify susceptible molecules revealed that only Slc5a10 (corresponding to SGLT5) showed >two-fold up-regulation in FRU versus GLU rats. RT-PCR and in situ hybridization confirmed the SGLT5 up-regulation (12 weeks GLU: 75.0 ± 5.8% vs. 12 weeks FLU: 230.1 ± 16.0%). Our findings may indicate that the high-fructose diet increased sodium reabsorption principally through up-regulated SGLT5, finally causing salt-sensitive hypertension.

The Horoscope trial aimed to assess the efficacy of home blood pressure (BP) telemonitoring (TLM) in controlling BP reduction in hypertensive patients compared with usual care. This is a multi-center, prospective randomized, parallel-group trial comparing TLM with usual care during a period of 6 months in patients with hypertension. We included 525 patients randomly assigned in a 1-1 ratio to telemonitoring (TLM group; n = 260) or usual care (control group; n = 265). After 6 months of follow up, mean values of 24-h systolic and diastolic blood pressure decreased in both TLM and control groups. The mean decrease was significantly greater in the TLM group vs control group (-3.29 mmHg Vs -1.19; p = 0.009) and (-2.9 mmHg Vs, -0.07; p = 0.002) for systolic and diastolic blood pressure, respectively. This study shows that TLM results in significant BP reduction compared to usual care in a Tunisian population of patients with hypertension. Our findings highlight the importance of integrating telemedicine in the management of hypertensive patients; it has the potential to improve the quality of the delivered care and to prevent cardiovascular consequences of uncontrolled BP.

The interplay between long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) in regulating hypertension modulate gene expression through different mechanisms, influencing key physiological and pathological processes. Specifically, interactions between lncRNAs and miRNAs affect various molecular pathways, including the renin-angiotensin-aldosterone system, which plays a critical role in blood pressure regulation. The lncRNA MALAT1 is particularly noted for its role in inflammation and oxidative stress regulation, suggesting potential targets for hypertension treatment and diagnostics. Interplay between lncRNAs and MicroRNAs in Hypertension.

KCNJ5 somatic mutations in aldosterone-producing adenoma (APA) are linked to higher left ventricular mass index (LVMI) and worse diastolic function. We previously identified an association between plasma tissue inhibitor of metalloproteinases-1 (TIMP-1) and an aldosterone-induced increase in LVMI and diastolic dysfunction. This study aimed to investigate the association between the presence of KCNJ5 somatic mutation and plasma TIMP-1 in APA patients. We enrolled 60 APA patients undergoing adrenalectomy, including 30 with KCNJ5 mutations (KCNJ5(+)) and 30 without (KCNJ5(-)). Clinical characteristics, echocardiographic data (including LVMI, inappropriately excessive LVMI (ieLVMI), and diastolic function) and plasma TIMP-1 levels were measured before surgery and 1 year postoperatively. The results showed that the KCNJ5(+) group had higher plasma TIMP-1 levels (P = 0.004) compared to the KCNJ5(-) group. The correlation between the KCNJ5 mutations and TIMP-1 levels remained significant after multiple regression analysis. To detect KCNJ5 mutations, receiver operating characteristic curve analysis showed TIMP-1 had the best area under the curve (AUC) value among various clinical parameters (AUC = 0.682, 95% confidence interval = 0.549-0.796, P = 0.008). Post-adrenalectomy, only the KCNJ5(+) group showed significant decrease in LVMI (P = 0.001) and log-transformed TIMP-1 levels (P = 0.035). Changes in ieLVMI before and after surgery were consistently correlated with changes in TIMP-1 levels in multivariable regression analysis. In conclusion, KCNJ5 somatic mutations in APA are associated with higher plasma TIMP-1 levels. In addition, TIMP-1 is an effective biomarker for detecting the presence of KCNJ5 mutations in APA patients.