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The sympathetic hyperactivity present in alpha2A/alpha2C-ARKO (show CYP19A1 ELISA Kits) mice alters vascular reactivity only in certain types of arteries
In summary, our results highlight the importance of alpha(2R) distribution within the NTS (show NTS ELISA Kits) regarding the neural control of blood pressure and the development of hypertension.
adrenaline inhibits insulin (show INS ELISA Kits) release through alpha(2A)- and alpha(2C)-adrenergic receptors via distinct intracellular signaling pathways
alpha2C adrenoceptor expression is permissive under Adra2c-NN in central (cerebral cortex, hippocampus, subthalamus, hypothalamus, superior colliculus, cerebellum, and brain stem) and peripheral (pancreatic beta-islets) tissues
mRNAs encoding the alpha(2A)-adrenergic receptor (show ADRA2A ELISA Kits) are up-regulated in the brainstem.
Local cooling-induced reduction of skin blood flow in mice primarily results from increased reactivity of alpha (2C)-adrenoceptors to circulating catecholamines, in which the Rho/Rho kinase (show ROCK2 ELISA Kits) pathway is involved.
Exercise training decreased alpha(2A)/alpha(2C)adrenoceptor lacking mice's cardiac angiotensin II levels and angiotensin-converting enzyme (show ACE ELISA Kits) activity.
Immunoreactivity for ADRA2C was densely distributed in vascular smooth muscle of nasal turbinates.
ADRA2c is associated with heart rate recovery after exercise.
Common polymorphisms in the ADRA2C gene are not associated with orthostatic hypotension risk in Chinese.
alpha2C-adrenoreceptor interaction with filamin-2 (show FLNC ELISA Kits)
Genetic variants of ADRA2C do not alter intracellular localization or plasma membrane trafficking.
the ADRA2C 322-325I/D genotype is a novel genetic risk marker for SBI among individuals with hyperhomocysteinemia.
The ADRA2A (show ADRA2A ELISA Kits) and ADRA2C polymorphisms did not contribute to an increased risk of ischemic stroke or any pathophysiological subtype
Bucindolol prevents ventricular arrhythmias in subjects with heart failure and reduced left ventricular ejection fractions, and this effect is modulated by adrenergic alpha 2 receptor (show ADRA2A ELISA Kits) polymorphisms.
the predicted signal peptide in the N-terminal tail of the alpha(2C)-adrenoceptor does not act as a cleavable signal peptide
The common ADRA2C variant affected pain perception before and after dexmedetomidine but did not affect other cognitive responses
Alpha-2-adrenergic receptors are members of the G protein-coupled receptor superfamily. They include 3 highly homologous subtypes: alpha2A, alpha2B, and alpha2C. These receptors have a critical role in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system. The mouse studies revealed that both the alpha2A and alpha2C subtypes were required for normal presynaptic control of transmitter release from sympathetic nerves in the heart and from central noradrenergic neurons. The alpha2A subtype inhibited transmitter release at high stimulation frequencies, whereas the alpha2C subtype modulated neurotransmission at lower levels of nerve activity. This gene encodes the alpha2C subtype, which contains no introns in either its coding or untranslated sequences.
, alpha-2C adrenergic receptor
, alpha-2C adrenoceptor
, alpha-2C adrenoreceptor
, adrenergic, alpha-2C-, receptor
, adrenergic receptor alpha-2C
, alpha-2B adrenergic receptor
, adrenergic receptor, alpha 2c
, alpha-2 adrenergic receptor subtype C4
, subtype alpha2-C4
, alpha-2C-adrenergic receptor
, Adrenergic alpha2C- receptor class I
, Adrenergic, alpha2C-, receptor class I
, alpha 2C adrenergic receptor