ATC Group: C02C Antiadrenergic agents, peripherally acting

The World Health Organization's ATC classification organizes medical drugs based on therapeutic properties, chemical composition, and anatomy. It helps make essential medicines readily available globally and is widely used in the pharmaceutical industry.

Position of C02C in the ATC hierarchy

Level Code Title
1 C Cardiovascular system
2 C02 Antihypertensives
3 C02C Antiadrenergic agents, peripherally acting

Group C02C contents

Code Title
C02CA Alpha-adrenoreceptor antagonists
C02CC Guanidine derivatives

Active ingredients in C02C

Active Ingredient

Betanidine is a post-ganglionic adrenergic neurone-blocking agent which exerts a marked postural hypotensive effect.

Doxazosin is a potent and selective post-junctional alpha-1-adrenoceptor antagonist. This action results in a decrease in systemic blood pressure.

Guanethidine is a antihypertensive drug. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues. It is taken up by norepinephrine transporters. It becomes concentrated in norepinephrine transmitter vesicles, replacing norepinephrine in these vesicles.

Indoramin is an alpha adrenoceptor blocking agent. It acts selectively and competitively on post-synaptic alpha-1 receptors, causing a decrease in peripheral resistance. It also produces relaxation of hyperplastic muscle in the prostate.

Prazosin causes a decrease in total peripheral vascular resistance through selective inhibition of postsynaptic alpha-1-adrenoreceptors in vascular smooth muscle. Prazosin has been found to successfully reduce the severity of the signs, symptoms, frequency and duration of attacks, in patients with Raynaud’s disease.

Urapidil is a α1-adrenoceptor antagonist and 5-HT1A receptor agonist and consequently inhibits the vasoconstrictor effect of catecholamines. It interacts with peripheral α1-adrenoceptors and central 5-HT1A receptors to produce vasodilation without sympathetic activation.

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