Alterations in osmotic but not pressor responses to ACTH by optic recess lesions in sheep

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):  
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

1982 ◽  
Vol 333 (1) ◽  
pp. 383-391
Author(s):  
Robert F. Bing ◽  
Gavin I. Russell ◽  
John D. Swales ◽  
Herbert Thurston
Keyword(s):  

2004 ◽  
Vol 56 (5) ◽  
pp. 756-762 ◽  
Author(s):  
Lijun Shi ◽  
Catalina Guerra ◽  
Jiaming Yao ◽  
Zhice Xu

1995 ◽  
Vol 58 (5) ◽  
pp. 583-587 ◽  
Author(s):  
Koichi Sato ◽  
Miho Sawada ◽  
Masayoshi Kojima ◽  
Yasuaki Dohi
Keyword(s):  

Author(s):  
Ryosuke Takeda ◽  
Abigail S.L. Stickford ◽  
Stuart A. Best ◽  
Jeung-Ki Yoo ◽  
Yu-Lun Liu ◽  
...  

Excessive salt intake is considered a risk factor for the development of hypertension. Additionally, aberrant neuro-circulatory responses to a cold stimulus are associated with an increased risk of hypertension. This study aimed to determine whether salt loading versus salt reduction would impact hemodynamic and sympathetic neural responses during the cold pressor test (CPT) in premenopausal women with a history of normal pregnancy. Nine healthy premenopausal women [42±3 (SD) yr] were given a standardized isocaloric high salt (HS; 250 mEq sodium/day) or low salt (LS; 50 mEq sodium/day) diet for 1-week each (~2 months apart with the order randomized), while water intake was ad libitum. Laboratory testing was performed following each HS and LS period in the mid-luteal phase of the menstrual cycle. Subjects were in the supine position and beat-by-beat blood pressure (BP), heart rate (HR) and muscle sympathetic nerve activity (MSNA) were continuously measured during 1-minute baseline followed by 2-minute CPT and 3-minute recovery. BP and HR increased during the CPT (both P<0.001); the responses were similar between HS and LS. MSNA increased during the CPT, but the increment (D) was greater during HS than LS (29±6 vs. 15±4 bursts/min; P<0.001). The transduction of MSNA for vasoconstriction during the CPT was lower in HS (P<0.05). Thus, salt loading augments sympathetic neural reactivity to the cold stimulus with similar pressor responses compared to salt reduction, which may be attributed to the blunted neurovascular transduction ─ a compensatory mechanism for hemodynamic homeostasis in premenopausal women with a history of normal pregnancy.


Sign in / Sign up

Export Citation Format

Share Document