How can vasoconstriction lower blood pressure
New therapeutic approach for salt-sensitive high blood pressure
Dr. Bettina Albers Press office of the German Hypertension League
German Hypertension League
A current publication  from the "Boston University School of Medicine" reports on new findings on the complex interplay between the sympathetic nervous system and the kidneys in the development of so-called salt-sensitive hypertension. The study was able to show for the first time that alpha1 adrenoreceptor blockers reduce the activity of the sodium reuptake process in the kidneys, thereby increasing salt excretion and thus lowering blood pressure. Ultimately, this also means that targeted therapy for salt-sensitive high blood pressure is available, which is a common reason why patients do not respond to conventional antihypertensive drugs.
In Germany, almost every third adult has high blood pressure (arterial hypertension). In the over 60-year-olds, on average, every second person is affected by increased values and thus has a significantly increased risk of life-threatening cardiovascular and vascular diseases (especially vascular calcifications / atherosclerosis). Heart attack and stroke are particularly feared secondary diseases, but years of high blood pressure can also lead to kidney failure or blindness.
It has long been known that consuming excessive amounts of table salt (sodium chloride) can increase the risk of developing hypertension. Salty foods create thirst, and salt binds water in the body. This increases the volume of fluid in the bloodstream - and with it the pressure in the blood vessels. Not all people are dependent on salt consumption and blood pressure, but many do. The cause is a special genetic predisposition (so-called salt sensitivity), but also additional diseases such as diabetes mellitus, kidney disease or disorders in the autonomic nervous system.
Patients with salt-sensitive high blood pressure typically have an 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"). The sympathetic neurotransmitter norepinephrine activates the alpha receptors of the blood vessels, which causes them to narrow (vasoconstriction) and thus increases blood pressure. It is also known that noradrenaline stimulates the renal sodium chloride cotransporter (NCC) in the cell membranes of the kidney tubules, so that more sodium is transported from the urine back into the blood. However, the exact mechanism by which norepinephrine affects renal sodium retention is not clear. Studies to investigate the adrenaline- or noradrenaline-controlled signaling pathways of the sympathetic nervous system that regulate NCC activity have so far not shown consistent results.
The well-known antihypertensive effect of alpha blockers consists in the vasodilating effect by relaxing the smooth vascular muscles (vascular dilation). The study was able to show for the first time that alpha1-adrenoreceptor blockers also reduce the activity of the sodium reuptake process and also lower blood pressure in this way. In their work, the researchers used selective alpha1-receptor blockers to investigate whether noradrenaline-dependent NCC activation is mediated via an alpha1-receptor-dependent signaling pathway in a salt-sensitive strain of rats. The salt intake of the animals was increased through the diet, whereupon the NCC activity and expression increased significantly and hypertension developed. Treatment with alpha1-receptor blockers resulted in a decrease in blood pressure - mediated by a decrease in NCC activity and NCC expression (i.e., lower NCC numbers on cell membranes), which prevented renal salt retention. The alpha1-receptor blockers were effective both when administered before the start of high salt intake and when salt-sensitive hypertension had already developed. Detailed molecular analyzes showed that in salt-sensitive hypertension (in contrast to strains of rats with salt-resistant normotonia) there is a disorder of the enzyme "WNK-Kinase 1/4" or a malfunction of the "WNK / SPAK / OxSR1" signaling pathway that the NCC -Activity regulated.
"These research results show how complex the pathomechanisms and relationships between the sympathetic nervous system and the kidneys are in the development of hypertension," comments Prof. Dr. med. Ulrich Wenzel, University Medical Center Hamburg-Eppendorf, CEO of DHL®. “Even if the exact pathomechanisms have not yet been clarified, selective alpha1-receptor blockers seem to be able to prevent salt-sensitive hypertension in a targeted manner. If these animal experimental findings are confirmed in clinical studies, this would be of great practical relevance, since these drugs could break the vicious circle and lead to normal blood pressure values in many people for whom conventional antihypertensive agents do not work (patients with so-called therapy-refractory hypertension). So far, we have only had the option of recommending to these patients to limit their salt intake to a minimum, which is anything but easy to implement because of the 'hidden salt' in many foods. Targeted therapy for salt-sensitive hypertension would help to ensure that significantly more patients could be brought into the target range with their blood pressure values and suffer fewer secondary diseases. "
 Franco Puleo F, Kim K, Frame AA et al. Sympathetic Regulation of the NCC (Sodium Chloride Cotransporter) in Dahl Salt-Sensitive Hypertension. Hypertension 2020 Nov; 76 (5): 1461-69
doi: 10.1161 / HYPERTENSIONAHA.120.15928. Epub 2020 Sep 28.
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