Hypertension, or high blood pressure, is a common cardiovascular condition with plenty of treatment options and prevention, such as prescribed ACE inhibitors or stress-reducing lifestyle. Recent research may have identified another possible drug target or even a new marker for hypertension.
A team from the Klinikum der Universitat in Germany was studying a protein called uromodulin. This protein is produced by cells in Henle’s Loop, which is involved in nutrient balance in the kidneys. Mutations in uromodulin can cause severe kidney disease but growing evidence of its association with cardiovascular health is what got the team’s attention.
Several studies have associated uromodulin with cardiovascular issues, but none have been able to reveal how it works. The team decided to conduct a new study to determine if uromodulin levels affected the common hypertension markers renin, aldosterone, or CT-proET-1. If they could link it to any of these, they had a start point for further investigation.
They began by gathering data from the KORA F4 study and analyzing the levels of uromodulin and hypertension markers. They noted that uromodulin levels were lower in hypertension patients, while renin and CT-proET-1 were significantly higher. This observation revealed an inverse relationship between uromodulin and both renin and CT-proET-1, pointing to a possible connection between them. There was no significant association of uromodulin with aldosterone.
The team states that the observations from this study support uromodulin as a protective molecule against hypertension. Uromodulin deficiency is significantly associated with hypertension. Some studies concur with this idea, but the team notes that other studies show high levels of uromodulin can also cause hypertension. The group proposed a mechanism by which loss of uromodulin, which coats Henle’s Loop, reducing the re-uptake of salts, triggers the renin-angiotensin-aldosterone system, causing hypertension.
The study concludes, “We demonstrate an inverse association of sUmod with arterial hypertension and with the vasoconstrictive prohormone CT-proET-1 in the population-based KORA F4 study. Thus, we provide indirect evidence for a systemic blood pressure regulative effect of sUmod.”