Preoptic–Periventricular Integrative Mechanisms Involved in Behavior, Fluid–Electrolyte Balance, and Pressor Responses

2013 ◽  
pp. 83-104
1980 ◽  
Vol 239 (5) ◽  
pp. R372-R376 ◽  
Author(s):  
G. D. Fink ◽  
W. J. Bryan

A small discrete area near the optic recess of the anterior ventral third ventricle (AV3V) in the rat brain has been shown to be an important mediator of cardiovascular and dipsogenic response to angiotensin II and osmotic stimuli and to be involved in normal day-to-day regulation of water and electrolyte balance. However, no attempt has been made until now to explore the function of the AV3V in species other than the rat. In the present study, rabbits subjected to electrolytic lesion of the AV3V exhibited expanded plasma volume and plasma sodium concentration, and significantly attenuated pressor responses to angiotensin II and hypertonic sodium chloride solutions injected via the lateral ventricles. Resting arterial pressure, plasma potassium concentration, extracellular fluid volume, and pressor responses to intravenous angiotensin II were not changed by lesioning. Thus, the effects of AV3V lesions in rabbits are similar, but not identical, to those previously observed in rats. Rabbits should be a suitable species in which to carry out studies aimed at distinguishing central and peripheral cardiovascular effects of angiotensin II.


Author(s):  
José Menani ◽  
Alexandre Vieira ◽  
Débora Colombari ◽  
Patrícia De Paula ◽  
Eduardo Colombari ◽  
...  

2020 ◽  
Vol 134 (19) ◽  
pp. 2581-2595
Author(s):  
Qiuhong Li ◽  
Maria B. Grant ◽  
Elaine M. Richards ◽  
Mohan K. Raizada

Abstract The angiotensin-converting enzyme 2 (ACE2) has emerged as a critical regulator of the renin–angiotensin system (RAS), which plays important roles in cardiovascular homeostasis by regulating vascular tone, fluid and electrolyte balance. ACE2 functions as a carboxymonopeptidase hydrolyzing the cleavage of a single C-terminal residue from Angiotensin-II (Ang-II), the key peptide hormone of RAS, to form Angiotensin-(1-7) (Ang-(1-7)), which binds to the G-protein–coupled Mas receptor and activates signaling pathways that counteract the pathways activated by Ang-II. ACE2 is expressed in a variety of tissues and overwhelming evidence substantiates the beneficial effects of enhancing ACE2/Ang-(1-7)/Mas axis under many pathological conditions in these tissues in experimental models. This review will provide a succinct overview on current strategies to enhance ACE2 as therapeutic agent, and discuss limitations and future challenges. ACE2 also has other functions, such as acting as a co-factor for amino acid transport and being exploited by the severe acute respiratory syndrome coronaviruses (SARS-CoVs) as cellular entry receptor, the implications of these functions in development of ACE2-based therapeutics will also be discussed.


Hypertension ◽  
1982 ◽  
Vol 4 (3) ◽  
pp. 154-158 ◽  
Author(s):  
B. A. Scoggins ◽  
J. P. Coghlan ◽  
M. Congiu ◽  
D. A. Denton ◽  
W. F. Graham ◽  
...  
Keyword(s):  

Author(s):  
Paola Rodriguez-Giustiniani ◽  
Nidia Rodriguez-Sanchez ◽  
Stuart D.R. Galloway

2021 ◽  
Author(s):  
Mazher Mohammed ◽  
Dominique N Johnson ◽  
Lei A Wang ◽  
Scott W Harden ◽  
Wanhui Sheng ◽  
...  

Abstract Aims These studies evaluate whether angiotensin type-2 receptors (AT2Rs) that are expressed on γ-aminobutyric acid (GABA) neurons in the nucleus of the solitary tract (NTS) represent a novel endogenous blood pressure-lowering mechanism. Methods and results Experiments combined advanced genetic and neuroanatomical techniques, pharmacology, electrophysiology, and optogenetics in mice to define the structure and cardiovascular-related function of NTS neurons that contain AT2R. Using mice with Cre-recombinase directed to the AT2R gene, we discovered that optogenetic stimulation of AT2R-expressing neurons in the NTS increases GABA release and blood pressure. To evaluate the role of the receptor, per se, in cardiovascular regulation, we chronically delivered C21, a selective AT2R agonist, into the brains of normotensive mice and found that central AT2R activation reduces GABA-related gene expression and blunts the pressor responses induced by optogenetic excitation of NTS AT2R neurons. Next, using in situ hybridization, we found that the levels of Agtr2 mRNAs in GABAergic NTS neurons rise during experimentally induced hypertension, and we hypothesized that this increased expression may be exploited to ameliorate the disease. Consistent with this, final experiments revealed that central administration of C21 attenuates hypertension, an effect that is abolished in mice lacking AT2R in GABAergic NTS neurons. Conclusion These studies unveil novel hindbrain circuits that maintain arterial blood pressure, and reveal a specific population of AT2R that can be engaged to alleviate hypertension. The implication is that these discrete receptors may serve as an access point for activating an endogenous depressor circuit.


1988 ◽  
Vol 254 (1) ◽  
pp. R75-R77
Author(s):  
D. Gazis ◽  
G. Gonzalez ◽  
M. Mendlowitz

The effects of the calcium channel blocker verapamil on simultaneously recorded uterine and pressor responses to the equipotent (in eliciting these responses) oxytocin-vasopressin analogue, oxypressin, were studied in urethan-anesthetized and pentolinium- and indomethacin-treated rats during injections and infusions of this analogue. Doses of verapamil that almost completely blocked the pressor response to infused oxypressin had no effect on a pressor response to injected oxypressin of equal magnitude. Larger doses of verapamil blocked the pressor response to injected oxypressin somewhat. Uterine responses were only marginally affected by these doses of verapamil, and there was no significant difference between infusion and injection or between estrus and diestrus.


Hypertension ◽  
2000 ◽  
Vol 36 (6) ◽  
pp. 1089-1092 ◽  
Author(s):  
Leonard F. Arnolda ◽  
Douglas J. McKitrick ◽  
Ida J. Llewellyn-Smith ◽  
Jane B. Minson

Sign in / Sign up

Export Citation Format

Share Document