Low-Density Lipoprotein Cholesterol And Angiotensin II Sensitivity!
Low-Density Lipoprotein (LDL) cholesterol, sometimes known as “bad” cholesterol, builds up in the blood vessel walls and increases our risk of developing health issues including a heart attack or stroke.
But cholesterol is not always harmful. To safeguard its neurons and produce healthy cells and hormones, our body requires it.
What Are The Effects Of Low-Density Lipoprotein?
Saturated fats raise our levels of “bad” LDL cholesterol, but foods high in fiber and Omega-3 fatty acids, such as whole grains, vegetables, fruits, nuts, and fatty fish, all lower it while also raising our levels of “good” HDL cholesterol.
Blood pressure is raised by a number of mechanisms by angiotensin II (Ang II), the most significant of which is vasoconstriction, sympathetic nervous system stimulation, enhanced aldosterone production, and renal effects.
Aside from these, Ang II also causes fibrosis, increased collagen type I and III production in fibroblasts, which thickens the vascular wall and myocardium, and promotion of growth, cell migration, and mitosis of vascular smooth muscle cells.
Losartan, an AT1 receptor-specific antagonist, has the potential to inhibit these activities because they are mediated by type 1 Ang II receptors (AT1).
High Cholesterol And Hypertension
High cholesterol and Hypertension are related. our arteries harden and narrow as a result of cholesterol plaque and calcium. As a result, pumping blood through them requires significantly more effort from our hearts. our blood pressure goes up too much as a result.
LDL cholesterol levels may rise as a result of some drugs. Some of these birth control methods, beta-blockers, thiazide diuretics, antiviral medications, anticonvulsants, retinoids, corticosteroids, and growth hormones are also included.
Low-density lipoprotein cholesterol (LDL-c) has a well-established involvement in the development of atherosclerosis. Additionally, angiotensin II (Ang II) possesses atherogenic characteristics.
It causes vascular cells’ decreased nicotinamide-adenine dinucleotide phosphate-oxidase to be stimulated and the Ang II type 1 (AT1) receptor to be activated, which produces superoxide and causes vascular hypertrophy, hyperplasia, and LDL oxidation.
Additionally, in hypercholesterolemic monkeys, an AT1-receptor antagonist prevented LDL oxidation and streak development. Animal and in vitro results support the hypothesis that elevated LDL-c is associated with higher expression of the AT1-receptor gene in vascular smooth muscle cells.
Relationship Between Angiotensin II And LDL Cholesterol
Angiotensin II and LDL cholesterol have both been found to worsen cardiovascular disease risk and severity.
Experiments have shown that vascular smooth muscle cells express more angiotensin type 1 (AT1) receptors in hypercholesterolemia, and human investigations have shown that this increases the vascular response to vasopressors.
In a young, normocholesterolemic population, the connection between the vascular response to angiotensin II (Ang II) infusion and serum levels of LDL-cholesterol in the systemic and renal circulation.
There is little proof that elevated LDL-c affects Ang II sensitivity in people directly. In earlier research, we looked at older individuals who also had cardiovascular risk factors like hypertension and metabolic syndrome, which could also account for the greater sensitivity to Ang II.
Evidence that LDL-c directly affects Ang II sensitivity may have implications for prevention. We reasoned that increased LDL-c levels would increase sensitivity to Ang II, and decreased LDL-c levels would, in turn, diminish this sensitivity.
The effect of fluvastatin on Ang II sensitivity was evaluated in the current randomized, double-blind, placebo-controlled crossover research in young, healthy people who have familial hypercholesterolemia (FH). A monogenetic condition called FH is characterized by significantly elevated LDL-c values.
It is generally known that patients with high cholesterol frequently have hypertension and that having both high cholesterol and high blood pressure increases the risk of developing cardiovascular disease.
The relationship between hypercholesterolemia and hypertension may be explained via vascular smooth muscle cells’ increased AT1 receptor expression.
Additionally, LDL-c-induced atherosclerosis and plaque instability, as well as the clinical symptoms of cardiovascular disease, may be accelerated by oxidative stress brought on by AT1-receptor stimulation.
To get to bodily cells, lipoproteins transport triglycerides, and cholesterol. The harmful cholesterol LDL, which clogs arteries, is eliminated by HDL (good cholesterol).
A gene results in elevated amounts of the artery-narrowing lipoprotein (a), or LP(a). Lipoprotein levels are determined using a lipid blood test.
Future studies are necessary to determine whether the normalization of Ang II sensitivity is linked to hypercholesterolemic persons’ more aggressive Low-Density Lipoprotein Cholesterol reduction.
A natural next step is to add-on treatment with medications that interfere with the renin-angiotensin system if, after aggressive cholesterol-lowering therapy, the recovery of Ang II sensitivity is still only partially complete.