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Intermitting... Although the here presented data are derived from a small number of subjects we could verify earlier findings of sunitinib treatment on blood pressure and on circulating endothelin-1 and VEGF levels.[5],[6] More importantly, it was enough powered to detect clear changes in skin sodium content and in plasma VEGF-C concentrations; sunitinib treatment decreased VEGF-C levels and led to an increase of skin sodium content. In contrast to VEGF-A, high baseline VEGF-C concentrations dropped after sunitinib treatment and stayed low independently from further treatment phase of sunitinib (Figure [F]). Our findings also suggest that whereas a side-effect such as blood pressure elevation is a reversible phenomenon of a sunitinib treatment, it could have a long-lasting effect on plasma VEGF-C concentrations and thereby on skin sodium homeostasis. [Extracted from the article]

High dietary salt intake is associated with hypertension; the prevalence of salt-sensitive hypertension increases with age. We hypothesized that tissue Na(+) might accumulate in hypertensive patients and that aging might be accompanied by Na(+) deposition in tissue. We implemented (23)Na magnetic resonance imaging to measure Na(+) content of soft tissues in vivo earlier, but had not studied essential hypertension. We report on a cohort of 56 healthy control men and women, and 57 men and women with essential hypertension. The ages ranged from 22 to 90 years. (23)Na magnetic resonance imaging measurements were made at the level of the calf. We observed age-dependent increases in Na(+) content in muscle in men, whereas muscle Na(+) content did not change with age in women. We estimated water content with conventional MRI and found no age-related increases in muscle water in men, despite remarkable Na(+) accumulation, indicating water-free Na(+) storage in muscle. With increasing age, there was Na(+) deposition in the skin in both women and men; however, skin Na(+) content remained lower in women. Similarly, this sex difference was found in skin water content, which was lower in women than in men. In contrast to muscle, increasing Na(+) content was paralleled with increasing skin water content. When controlled for age, we found that patients with refractory hypertension had increased tissue Na(+) content, compared with normotensive controls. These observations suggest that (23)Na magnetic resonance imaging could have utility in assessing the role of tissue Na(+) storage for cardiovascular morbidity and mortality in longitudinal studies. [ABSTRACT FROM AUTHOR]

The article presents a study on the relationship between dietary salt intake and hypertension. The study involves the use of quantitative sodium magnetic resonance imaging (Na-MRI) in visualizing Na+ in the skin and soft tissues. The noninvasive quantification of Na+ concentrations in the skin and skeletal muscle in humans using Na-MRI is cited as an key finding of the study. Results indicate an increase in Na+ storage in patients with refractory hypertension.

Hypertension is linked to disturbed total-body sodium (Na(+)) regulation; however, measuring Na(+) disposition in the body is difficult. We implemented (23)Na magnetic resonance spectroscopy ((23)Na-MR) and imaging technique ((23)Na-MRI) at 9.4T for animals and 3T for humans to quantify Na(+) content in skeletal muscle and skin. We compared (23)Na-MRI data with actual tissue Na(+) content measured by chemical analysis in animal and human tissue. We then quantified tissue Na(+) content in normal humans and in patients with primary aldosteronism. We found a 29% increase in muscle Na(+) content in patients with aldosteronism compared with normal women and men. This tissue Na(+) was mobilized after successful treatment without accompanying weight loss. We suggest that, after further refinements, this tool could facilitate understanding the relationships between Na(+) accumulation and hypertension. Furthermore, with additional technical advances, a future clinical use may be possible. [ABSTRACT FROM AUTHOR]

Introduction: Renal denervation has been shown to be effective in patients with hypertension. Recently, we found that afferent renal neurons show a distinctive feature, exhibiting predominantly a sustained firing upon current injection due to a specific expression of TTX resistant Na-channels. So far, the activity of these specific sensory neurons in hypertension is unclear. Hence we wanted to test the hypothesis that the firing pattern of renal afferent neurons is altered in the 2K/1C model of hypertension.Methods: Hypertension was induced by unilateral clipping of the renal artery in Sprague Dawley rats 3 weeks prior to experiments. Blood pressure was confirmed by an intraarterial measurement. Retrograde labelling (DiI) allowed the identification of renal afferent neurons in the Dorsal root ganglion (DRG Th11-L2). Current clamp was used to characterize neurons as “tonic”, i.e. sustained action potential (AP) firing or “phasic”, i.e. <5 APs according to their firing upon current injections. Electrophysiological parameters and AP properties were determined in neurons of hypertensive animals and controls. Renal morphology was investigated.Results: Renal DRG neurons of hypertensive animals (n=88) showed a significant decrease in tonic firing pattern compared to controls (n=84) (44.3% [39/88] vs. 59.5% [50/84], p< 0.05). Current Clamp analysis revealed no significant change in action potential shape in hypertensive animals (overshoot, firing threshold, AP- duration). Tonic cells revealed a higher capacity in hypertensive rats (124pF vs. 87.8pF, p<0.01), all other parameters (resting potential, resistances) were equal in both groups. No differences in renal pathomorphology could be observed between clipped and non-clipped kidney in hypertensive animals. (BP: 187.5 mmHg versus controls: 106.5mmHg)Conclusion: Hence the excitability of afferent renal neurons in a model of renovascular hypertension is significantly altered, as renal afferent DRG neurons exhibit less sustained firing upon stimulation. Sustained high blood pressure is possibly rather characterized by a generally decreased afferent renal activity with impaired sympathoinhibition than by activated sympathoexcitatory fibers from the clipped kidney. [ABSTRACT FROM AUTHOR]

Hypertension is the most common cardiovascular risk factor and systolic blood pressure increases continuously with age. Increased vascular stiffness, nitric oxide, renin-angiotensin aldosterone system and salt intake have been implicated. We have developed 23Na magnetic resonance imaging (23Na MRI) and showed that aldosterone influences tissue Na+ storage. We reasoned that Na+ might accumulate in tissues with age. We investigated tissue Na+ of the lower leg in 113 subjects with 3T 23Na MRI. Tissue Na+ concentration was calibrated by solutions containing 10 to 40 mmol/l of Na+. Prior to 23Na MRI measurements, a medical history was taken, blood and urine samples were obtained and blood pressure was analyzed in seated position. The age of the 113 subjects analyzed by 23Na MRI ranged from 22 to 90 years. We studied 44 women and 69 men. Hypertension was diagnosed in 46 subjects (29 men and 17 women). Men showed an exponential increase in tissue Na+ with age (muscle R2 = 0.54, skin R2= 0.33). In contrast, tissue Na+ in women was only slightly affected by age and increased linearly (skin R2 = 0.40, muscle R2= 0.13). To compare subpopulations, we allocated the participants into three different age groups <50, 50-65 and >65 years. A gender difference in skin tissue Na+ could be found throughout all groups with higher levels in men (14.3 vs. 18.1 (<50 yrs), 19.0 vs. 24.5 (50-65 yrs), 20.1 vs. 27.4 mmol/l (>65 yrs); p < 0.05). Skin Na+ content was elevated in hypertensive women compared to age-matched controls (17.2, n = 12 vs. 21.0 mmol/l, n = 17; p<0.05). We could not identify such a difference in hypertensive versus normotensive men. In line with our previous results, older hypertensive patients receiving an aldosterone antagonist revealed muscle Na+ values below age-matched subjects (17.6, n = 6 vs. 21.3 mmol/l, n = 24; p < 0.05). We conclude that aging is associated with Na+ tissue accumulation with a pronounced gender difference. Skin Na+ overload occurs in hypertensive women but not in men. Aldosterone antagonists may reset the age-dependent muscle Na+ overload to levels of young healthy controls. [ABSTRACT FROM AUTHOR]