From the Guidelines
Vascular smooth muscle contraction is primarily mediated by calcium ions (Ca2+) entering vascular smooth muscle cells through voltage-dependent L- and T-type calcium channels, as stated in the study by 1. This process is crucial for the regulation of blood vessel diameter and blood pressure. The calcium ions enter the cells and initiate contraction by calcium-induced intracellular Ca2+ release from the sarcoplasmic reticulum. Some key points to consider about vascular smooth muscle contraction include:
- Calcium ions play a major role in the contraction of vascular smooth muscle cells, as well as in the inotropic and chronotropic functions of the heart 1.
- The dihydropyridine calcium channel blockers (CCBs) are highly selective for arterial/arteriolar tissues and cause vasodilation by binding to a common site on the 1-subunit of the L-type channel 1.
- The nondihydropyridine CCBs have greater effects on the atrioventricular node than on the sinoatrial node and may predispose to high-degree atrioventricular block when administered to patients with preexisting atrioventricular nodal disease or when given with other agents 1. The regulation of vascular smooth muscle contraction is complex and involves various factors, including sympathetic nervous system activity, hormones, and local factors. Some of the key factors that regulate vascular smooth muscle contraction include:
- Sympathetic nervous system activity (via norepinephrine)
- Hormones like angiotensin II and vasopressin
- Local factors such as endothelin-1 (constricting) and nitric oxide (relaxing) Understanding the mechanism of vascular smooth muscle contraction is essential for comprehending hypertension pathophysiology and the action of antihypertensive medications, as discussed in the study by 1.
From the Research
Vascular Smooth Muscle Contraction Mechanisms
- Vascular smooth muscle contraction is triggered by an increase in intracellular free calcium concentration ([Ca2+]i), promoting actin-myosin cross-bridge formation 2
- Contraction is also regulated by calcium-independent mechanisms involving RhoA-Rho kinase, protein Kinase C and mitogen-activated protein kinase signalling, reactive oxygen species, and reorganization of the actin cytoskeleton 2, 3
- The smooth muscle cell directly drives the contraction of the vascular wall and hence regulates the size of the blood vessel lumen 4
Regulation of Vascular Smooth Muscle Contraction
- Vascular smooth muscle function is regulated by complex-interacting systems such as the renin-angiotensin-aldosterone system, sympathetic nervous system, immune activation, and oxidative stress 2
- Activation of immune/inflammatory pathways and non-coding RNAs are also emerging as important regulators of vascular function 2
- Ca2+ has been established as a major regulator of VSM contraction, and its sources, cytosolic levels, homeostatic mechanisms and subcellular distribution have been defined 3
Pathological Conditions
- Abnormal contractions can cause and or contribute to pathology such as hypertension, ischemia and infarction 5
- Hypertension is a multifactorial disease with many causes and a profound impact on the cardiovascular system 2, 5
- Vascular smooth muscle cell [Ca2+]i not only determines the contractile state but also influences activity of many calcium-dependent transcription factors and proteins thereby impacting the cellular phenotype and function 2
Treatment of Vascular Smooth Muscle Disorders
- Modulators of [Ca2+]c, PKC and ROCK activity could be useful in mitigating the increased vasoconstriction associated with vascular disease 3
- Diuretics and calcium-blocking drugs are more effective in elderly patients at lowering systolic blood pressure 6
- Combination therapy will usually be required to achieve goal blood pressure in elderly people with essential hypertension 6