Almost every third adult in Germany has high blood pressure (arterial hypertension). According to the Heart Foundation, on average every second person over 60 years of age is affected by elevated values and thus has a significantly increased risk of life-threatening cardiovascular and vascular diseases (especially vascular calcification/atherosclerosis). Particularly dreaded secondary diseases are heart attacks and strokes, but years of high blood pressure can also lead to kidney failure or blindness.
In a recent announcement, the German Hypertension League refers to a publication of the “Boston University School of Medicine” published in the journal “Hypertension”, which reports on new findings on the complex interaction of the sympathetic nervous system and the kidneys in the development of so-called salt-sensitive hypertension. Their findings could contribute to a targeted therapy for salt sensitive hypertension, which is a common reason why patients do not respond to conventional antihypertensives.
Experts repeatedly warn against high salt consumption, as it is one of the most important risk factors for high blood pressure (hypertension). But people react very differently to salt. Particularly among those who are sensitive to salt, blood pressure rises if they consume too much table salt. In these people, antihypertensive drugs often do not work as well. But researchers are now reporting on a new therapeutic approach for salt-intensive hypertension sufferers.
New therapy for salt-sensitive hypertension
It has long been known that the consumption of excessive amounts of common salt (sodium chloride) can increase the risk of developing hypertension. Nevertheless, the average salt consumption of Germans is much too high. According to the German Society for Nutrition (DGE), an orientation value of up to six grams of table salt per day is given for the intake of table salt. This amount corresponds to approximately one teaspoonful. But in this country the food salt supply lies with approximately 70 per cent of the women and with approximately 80 per cent of the men over it.
Salty foods make you thirsty, and salt also binds water in the body. As a result, the volume of fluid in the bloodstream increases – and with it the pressure in the blood vessels, explain the experts from the Heart Foundation. Although not everyone is dependent on salt consumption and blood pressure, many people are. This is due to a special genetic predisposition (so-called salt sensitivity), but also to additional diseases such as diabetes mellitus, kidney disease or disorders of the autonomic nervous system.
Patients with salt sensitive hypertension typically have increased activity of the sympathetic nervous system (sympathetic nervous system) and their kidneys retain too much salt instead of excreting it with the urine (renal “sodium retention”). According to the data, the sympathetic messenger substance (neurotransmitter) noradrenaline activates the alpha-receptors of the blood vessels, which causes their constriction (vasoconstriction) and thus increases blood pressure.
High blood pressure due to too much salt
It is also known that noradrenaline stimulates the renal sodium chloride cotransporter (NCC) in the cell membranes of the renal tubules, so that more sodium is transported from the urine back into the blood. However, the exact mechanism by which norepinephrine influences renal sodium retention is not known. Scientific studies investigating the adrenaline- or noradrenaline-controlled signaling pathways of the sympathetic nervous system that regulate NCC activity have not yet yielded consistent results.
The known blood pressure-lowering effect of so-called alpha-blockers consists in the vasodilating effect by slackening of the smooth vascular muscles (vascular dilatation). In the current study it could be shown for the first time that alpha1-adrenoreceptor blockers additionally reduce the activity of the sodium reuptake process and also lower blood pressure in this way.
As stated in the communication, the animals’ dietary salt intake was increased, resulting in a significant increase in NCC activity and expression and the development of hypertension. Treatment with alpha-1 receptor blockers then resulted in a reduction in blood pressure – mediated by a decrease in NCC activity and NCC expression (i.e. lower NCC levels on cell membranes), which prevented renal salt retention.
In their work, the researchers used selective alpha1-receptor blockers to investigate whether noradrenalin-dependent NCC activation is mediated by an alpha1-receptor-dependent signaling pathway in a salt sensitive rat strain.
“These research results show how complex the pathomechanisms and interrelationships of the sympathetic nervous system and the kidneys are in the development of hypertension,” commented Prof. Dr. med. Ulrich Wenzel, University Medical Center Hamburg-Eppendorf (UKE), Chairman of the Board of Directors of DHL. “Even though the exact pathomechanisms are not yet understood, selective alpha1-receptor blockers seem to be able to specifically prevent salt-sensitive hypertension,” the expert added.
“If these animal experimental findings are confirmed in clinical studies, this would be of great practical relevance, as these drugs could break the vicious circle and lead to normal blood pressure values in many people in whom conventional antihypertensive drugs do not work (patients with so-called therapy-refractory hypertension),” Professor Wenzel emphasizes. Up to now, he says, the only way to date has been to recommend that these patients limit their saline intake to a minimum, but this is anything but easy to implement, partly because of “hidden salt” in many foods.
Alpha1-receptor blockers were effective both when administered before starting high salt intake and in cases of already developed salt-sensitive hypertension. Detailed molecular analyses revealed that in salt sensitive hypertension (in contrast to rat strains with salt resistant normotension) there is a disorder of the enzyme “WNK kinase 1/4” or a malfunction of the “WNK/SPAK/OxSR1” signaling pathway that regulates NCC activity, the researchers report.
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