Chlorphenamine

UNDER REVIEW (September 2016)

Mechanism of Action:

Competitively blocks the effects of histamine at peripheral histamine H1 receptor sites.

 

Montelukast

UNDER REVIEW (September 2016)

Mechanism of Action:

Cysteinyl-leukotriene receptor antagonist, anti-inflammatory action [leukotriene antagonist]. Leukotriene such as LTC4 and LTD4 are spasmogens (cause smooth muscle in airways to contract and become “twitchy” or hypersensitive).

Lecture and CAL materials:

Ipratropium

UNDER REVIEW (September 2016)

Mechanism of Action:

Ipratropium is an antagonist at muscarinic acetylcholine receptors (mAChR)(m3 subtype). Muscarinic AChRs are transmembrane G-protein coupled receptors (GPCRs) which are activated by the endogenous neurotransmitter, acetylcholine, the key transmitter in the parasympathetic nervous system, and also a major transmitter in the CNS. Another well-known muscarinic antagonist is atropine.

Lecture and CAL materials:

Theophylline

UNDER REVIEW (September 2016)

Mechanism of Action:

Theophylline is a xanthine derivative drug that has a structural and pharmacological similarity to caffeine. It is naturally found in black tea and green tea. The mechanism of action is probably by inhibition of phosphodiesterase (PDE), an enzyme that breaks down the secondary messenger cyclicAMP. Potentiation of cAMP, the secondary messenger for beta-adrenoreceptors, leads to smooth muscle relaxation. Some of the effects of theophylline are therefore similar to beta-agonists. The main actions of theophylline are (1) relaxation of bronchial smooth muscle, (2) positive inotropic – increases heart muscle contractility and efficiency(3) positive chronotropic – increases heart rate, (4) lowers blood pressure, (5) increases renal blood flow, and (6) some anti-inflammatory effect. Theophylline may also antagonise the effects of adenosine.

Lecture and CAL materials:

Adrenaline

UNDER REVIEW (April 2017)

Mechanism of Action:

Beta-1 and beta-2 adrenoreceptor agonist, alpha adrenoceptor agonist. Beta and alpha adrenoceptors are 7TM G-protein coupled receptors (GPCRs). Occupation of cardiac beta1 adrenoreceptors (by the endogenous ligand, noradrenaline, released from sympathetic [(nor)adrenergic] nerve endings; or by the circulating hormones adrenaline and noradrenaline, reflexly released into blood by the adrenal medulla; or by injected adrenaline) acts via G-protein-coupled activation of adenylate cyclase, which increases cAMP, leading to activation of protein kinase A (PKA). In the heart PKA phosphorylates Ca2+ channels, increasing inward Ca2+ current and hence force of contraction. Also get increased heart rate and electrical excitability. Adrenaline is also an aplha-adrenoceptor agonist, causing vasocontriction and a rise in mean BP via constriction of resitance vessels (arterioles).

Lecture and CAL material:

Salbutamol

UNDER REVIEW (September 2016)

Mechanism of Action:

Salbutamol is a short acting beta-2 adrenoceptor agonist. Activation of beta-2 receptors relaxes bronchial smooth muscle, relaxes myometrial smooth muscle in uterus, causes tremor of skeletal muscle and tends to stimulate uptake of potassium into cells. Beta-2 receptors (transmembrane G-protein coupled receptors) are normally activated by circulating adrenaline (hormone, released from adrenal medulla). Salbutamol is not entirely specific and has slight cross-reactivity with beta-1 adrenoceptors leading to tachycardia and increased force of cardiac contraction (generally only seen with very high doses). Beta-2 receptors also mediate vasodilatation, glycogenolysis, lipolysis and are found on cells of the immune system.

Lecture and CAL materials:

Oxygen

UNDER REVIEW (September 2016)

Mechanism of Action:

Oxygen is a naturally occurring gas that is vital for life in all aerobic cells. Its tetravalent reduction to water in the mitochondrial electron transport chain provides the energy for all cellular activities. It is normally found at a partial pressure of 13KPa in arterial blood which is equivalent to 99% saturation of haemoglobin. In several cardiac and respiratory disease states gas exchange in the lung is impaired leading to arterial hypoxaemia. This reduction in oxygen carriage and delivery to cells can be partially reversed by increasing the inspired oxygen concentration above the 20% found in room air with supplementary oxygen. Oxygen should be regarded as a drug.

Lecture and CAL materials: