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The beta-2 adrenergic receptor (β 2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-adrenergic receptor that binds epinephrine (adrenaline), a hormone and neurotransmitter whose signaling, via adenylate cyclase stimulation through trimeric G s proteins, increases cAMP, and, via downstream L-type calcium channel interaction, mediates physiologic responses such as smooth ...
Beta 2-adrenergic agonists, also known as adrenergic β 2 receptor agonists, are a class of drugs that act on the β 2 adrenergic receptor. Like other β adrenergic agonists , they cause smooth muscle relaxation. β 2 adrenergic agonists' effects on smooth muscle cause dilation of bronchial passages , vasodilation in muscle and liver ...
When NE is released into the synapse, it feeds back on the α 2 receptor, causing less NE release from the presynaptic neuron. This decreases the effect of NE. There are also α 2 receptors on the nerve terminal membrane of the post-synaptic adrenergic neuron. Actions of the α 2 receptor include: decreased insulin release from the pancreas [19]
Vascular smooth muscle contracts or relaxes to change both the volume of blood vessels and the local blood pressure, a mechanism that is responsible for the redistribution of the blood within the body to areas where it is needed (i.e. areas with temporarily enhanced oxygen consumption).
A 2014 meta-analysis found that unlike non-selective beta-blockers, β 1 selective beta-blockers (bisoprolol) showed only a small impact on lung function, with patients remaining responsive to salbutamol (β 2-agonist) rescue therapy and endorses the use of bisoprolol in select patients with controlled asthma.
Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; [1] this may be measured by echocardiography or cardiac catheterization.
Basic therapy can lead to dramatic clinical improvements in patients with right heart failure by instituting diuretic therapy. This reduces the right ventricular preload. Moreover, high-dose calcium-channel blockers among patients who have a response to this treatment can prolong survival and improve pulmonary haemodynamics.
Aging causes mutations in protein folding, and as a result causes deposits of abnormal modified proteins to accumulate in specific areas of the brain. In Alzheimer's, deposits of Beta-amyloid and hyperphosphorylated tau protein form extracellular plaques and extracellular tangles. [14]