Antihypertensive and neuroprotective effects of catestatin in spontaneously hypertensive rats: Interaction with GABAergic transmission in amygdala and brainstem

Catestatin and orexin-A influence hamster thermic states during hibernation

“…Concomitantly, hypothalamic neuronal fields enriched with elevated ORX2R expression levels supplied a notable reduction of neurodegenerative signals especially after treatment with CST and this is in good agreement with the results of another study 6 as well as with the longer neuronal survival induced by such an orexinergic subtype in some limbic areas 2 . However, despite the potent sympathoinhibitory and antihypertensive effects of CST causing a marked decrease of blood pressure following infusion into the central amygdalar nucleus, it seems to accomplish such a feature via the major inhibitory receptor GABA A complex of this limbic region as illustrated in another hypertensive model, i.e., the spontaneously hypertensive rat 7 . It is noteworthy that chromogranin A-enriched brain areas surrounded by GABA A interneurons have pointed to this neuroreceptor as an important neuronal element responsible for stress-dependent hemodynamic dysfunctions.…”

“…It is noteworthy that chromogranin A-enriched brain areas surrounded by GABA A interneurons have pointed to this neuroreceptor as an important neuronal element responsible for stress-dependent hemodynamic dysfunctions. In this particular case, the inhibition of GABA A receptors by its major antagonist bicuculline completely abolishing CST-induced sIPSC along with the chromogranin A-derived peptide neuroprotective effects tend to be responsible for the onset of CST sympathoinhibitory and antihypertensive actions 2 , 7 . As far as α 1 , a main GABA A receptor subunit is concerned, it seems to guarantee varying degrees of anti-sedative sensitivities during homeostatic events and exerts protection against metabolic-/temperature-dependent sleeping and motor difficulties.…”

Gamma-Aminobutyric Acid Increases Erythropoietin by Activation of Citrate Cycle and Stimulation of Hypoxia-Inducible Factors Expression in Rats

“…It is produced by decarboxylation of glutamate by the enzyme glutamate decarboxylase and is metabolized by transamination via the catalyzing effects of GABA transaminase to yield succinic semialdehyde or succinic acid [5,6]. GABA is defined as an inhibitory neurotransmitter in the central nervous system [7] and has various positive effects on mammalian physiology, including reducing blood pressure, relieving anxiety, and enhancing immunity [8][9][10][11].…”

“Unclassical” Combination of Smell Dysfunction, Altered Abdominal Nociception and Human Hypertension Associated “Classical” Adrenal-Augmentation

“…When neuroendocrine neoplasm like the one reported here appears, secretion of autocrine growth factors through voltage-sensitive L-type calcium channels [33] is implicated in the aberrant spinal processing of nociception mediated by nanoproteins such as CGA. To remark, CGA-associated function and dysfunction is mediated at the brainstem level, mainly over a region that encircles the nucleus of the tractus solitarius [34], which is strongly synaptophysin reactive [35], and it is heavily involved in autonomic regulation under normal conditions [36]. These mechanisms are paradoxically altered under pathological and stressful situations [37-39].…”