A New Target Mechanism for Lowering Blood Pressure in Cases of Hypertension
Hypertension, high blood pressure, is caused by arterial stiffness, which is in turn caused by a combination of mechanisms such as the accumulation of persistent cross-links that alter the structural properties of tissue, and chronic inflammation produced by senescent cells that alters the behavior of cells in blood vessel walls. Hypertension damages fragile tissues, causes the muscle of the heart to become larger and weaker, and ultimately interacts with the corrosive effects of atherosclerosis on blood vessel walls to produce a fatal rupture, leading to a stroke or heart attack.
The work noted here is representative of most efforts to safely lower blood pressure, in that it attempts to force cellular mechanisms in blood vessel walls into a more functional state without addressing the underlying causes of dysfunction - those that stiffen blood vessels. All too much of medical research has this focus: tinker with cell state in patients, but don't repair the damage that is causing those cells to run awry.
In the case of raised blood pressure, however, this condition directly causes a varied package of downstream harm, and is an important mediating mechanism between low-level molecular damage and high-level structural consequences to organs. So it is possible to make some progress, produce some degree of benefits to patients, by lowering blood pressure without addressing the causes of hypertension. That doesn't make it the best strategy, and it certainly shouldn't be the most effective approach. That most effective approach would have to involve repair of molecular damage that in turn reverses arterial stiffening.
Researchers have demonstrated that Galectin-1, a protein in our body, influences the function of another protein known as L-type (Cav1.2) calcium channel found on the arteries that normally acts to contract the blood vessels. By reducing the activity of these calcium channels, Galectin-1 is able to lower blood pressure.
Hypertension is a common problem worldwide. Importantly, age is a major risk factor for the development of hypertension. According to the World Health Organization, elevated blood pressure is estimated to cause 7.5 million deaths globally, which represents more than 12 per cent of the total of all deaths. This is because hypertension is associated with major killers like coronary heart diseases and stroke. In addition, hypertension can also cause renal impairment, retinal haemorrhage, and visual impairment.
As hypertension is a common denominator to many serious conditions described above, nipping the problem at its bud will significantly improve our health. Although patients with Stage I hypertension are mostly recommended to make lifestyle changes to reduce the risks of suffering other cardiovascular diseases, those with Stage 2 hypertension or above have to take anti-hypertensive medicines to control blood pressure.
Calcium channel blockers (CCB) are traditionally used in the clinics to lower blood pressure, but the use of such medications was reported to be associated with increased risk for heart failure in hypertensive patients particularly those with heart problems due to their bad side effects. Therefore, the development of drugs that could adjust the activity of L-type (CaV1.2) calcium channel, rather than blocking its normal function altogether, has emerged as a novel research direction for anti-hypertensive therapeutics. The discovery that Galectin-1 can perform such a desired function represents a pathway to control blood pressure. The good news is that Galectin-1 only targets L-type (CaV1.2) calcium channel in the blood vessels. It spares other types of calcium channels that are important for the general functions of our body.
"The reported effects of Galectin-1 protein, and of its analogues, on the blood pressure in various models of human arteries and the circulatory system are encouraging. The results suggest that there is a reasonable likelihood of fabricating an antihypertensive treatment-molecule, based on Galectin-1, which will consistently suppress, without negating, the Cav1.2 calcium channel in human arteries, so lowering the blood pressure in persons with pulmonary hypertension. The results from human pulmonary arteries suggest that the candidate treatment-molecule might also be useful in the condition known as pulmonary arterial hypertension, for which highly cost-effective drugs are lacking."
on a similar note (open access):
The matrix proteins aggrecan and fibulin-1 play a key role in determining aortic stiffness
http://www.nature.com/articles/s41598-018-25851-5