Optical perturbation of Agtr1a-containing neurons and afferents within the caudal nucleus of the solitary tract modulates sodium intake.

Angiotensin-II (Ang-II) production is driven by deviations in blood volume and osmolality, and serves the role of regulating blood pressure and fluid intake to maintain cardiovascular and hydromineral homeostasis. These actions are mediated by Ang-II acting on its type 1a receptor (AT1aR) within the central nervous system and periphery. Of relevance, AT1aR are expressed on sensory afferents responsible for conveying cardiovascular information to the nucleus of the solitary tract (NTS).

Angiotensin-(1-5) is a Potent Endogenous Angiotensin AT -Receptor Agonist.

Background: The renin-angiotensin system involves many more enzymes, receptors and biologically active peptides than originally thought. With this study, we investigated whether angiotensin-(1-5) [Ang-(1-5)], a 5-amino acid fragment of angiotensin II, has biological activity, and through which receptor it elicits effects.

Methods: The effect of Ang-(1-5) (1µM) on nitric oxide release was measured by DAF-FM staining in human aortic endothelial cells (HAEC), or Chinese Hamster Ovary (CHO) cells stably transfected with the angiotensin AT -receptor (AT R) or the receptor Mas.

Alleviating Hypertension by Selectively Targeting Angiotensin Receptor-Expressing Vagal Sensory Neurons.

Cardiovascular homeostasis is maintained, in part, by neural signals arising from arterial baroreceptors that apprise the brain of blood volume and pressure. Here, we test whether neurons within the nodose ganglia that express angiotensin type-1a receptors (referred to as NG) serve as baroreceptors that differentially influence blood pressure (BP) in male and female mice. Using -Cre mice and Cre-dependent AAVs to direct tdTomato to NG, neuroanatomical studies revealed that NG receive input from the aortic arch, project to the caudal nucleus of the solitary tract (NTS), and synthesize mechanosensitive ion channels, To evaluate the functionality of NG, we directed the fluorescent calcium indicator (GCaMP6s) or the light-sensitive channelrhodopsin-2 (ChR2) to -containing neurons.

Fatigue in young patients with acquired brain injury in the outpatient rehabilitation setting: A 2-year follow-up study.

Acquired brain injury (ABI) may cause fatigue and participation restrictions in young patients. However, knowledge regarding the course of these problems over time is lacking. This study aims to describe the course of fatigue and participation and their relationship over time in an observational two-year follow-up study among patients(5-24 years) with ABI referred for outpatient rehabilitation and their parents.