scholarly journals Sodium Sensitivity of Arterial Blood Pressure in L-NAME Hypertensive but not eNOS Knockout Mice

2006 ◽  
Vol 19 (3) ◽  
pp. 327-329 ◽  
Author(s):  
D MATTSON ◽  
C MEISTER
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Knockout Mice ◽  
Sodium Sensitivity ◽  
Arterial Blood

scholarly journals Arterial Blood Pressure and Renal Sodium Excretion in Dopamine D3 Receptor Knockout Mice

2007 ◽  
Vol 30 (1) ◽  
pp. 93-101 ◽  
Author(s):  
Torsten STAUDACHER ◽  
Bärbel PECH ◽  
Michael TAPPE ◽  
Gerhard GROSS ◽  
Bernd MÜHLBAUER ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Knockout Mice ◽  
Sodium Excretion ◽  
Dopamine D3 Receptor ◽  
D3 Receptor ◽  
Arterial Blood ◽  
Renal Sodium Excretion ◽  
Dopamine D3

A new index of sodium sensitivity risk from arterial blood pressure monitoring during habitual salt intake

2013 ◽  
Vol 168 (4) ◽  
pp. 4523-4525 ◽  
Author(s):  
Paolo Castiglioni ◽  
Gianfranco Parati ◽  
Lorenzo Brambilla ◽  
Valerio Brambilla ◽  
Massimo Gualerzi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Salt Intake ◽  
Blood Pressure Monitoring ◽  
Pressure Monitoring ◽  
Sodium Sensitivity ◽  
Arterial Blood

scholarly journals Larger Anastomoses in Angiotensinogen-Knockout Mice Attenuate Early Metabolic Disturbances after Middle Cerebral Artery Occlusion

1999 ◽  
Vol 19 (10) ◽  
pp. 1092-1098 ◽  
Author(s):  
Keiichiro Maeda ◽  
Ryuji Hata ◽  
Michael Bader ◽  
Thomas Walther ◽  
Konstantin-Alexander Hossmann
Keyword(s):  
Blood Pressure ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Knockout Mice ◽  
Therapeutic Window ◽  
Wild Type ◽  
Arterial Blood ◽  
Mca Occlusion

Abnormalities in the homeostasis of the renin-angiotensin system have been implicated in the pathogenesis of vascular disorders, including stroke. The authors investigated whether angiotensinogen (AGN) knockout mice exhibit differences in brain susceptibility to focal ischemia, and whether such differences can be related to special features of the collateral circulation. Wild-type and AGN-knockout mice were submitted to permanent suture occlusion of the middle cerebral artery (MCA). The collateral vascular system was visualized by systemic latex infusion, and the ischemic lesions were identified by cresyl-violet staining. The core and penumbra of the evolving infarct were differentiated by bioluminescence and autoradiographic imaging of A TP and protein biosynthesis, respectively. In wild-type mice, mean arterial blood pressure was 95.0 ± 8.6 mm Hg, and the diameter of fully relaxed anastomotic vessels between the peripheral branches of the anterior and middle cerebral arteries 26.6 ± 4.0 μm In AGN knockouts, mean arterial blood pressure was significantly lower, 71.5 ± 8.5 mm Hg ( P <,01), and the anastomotic vessels were significantly larger, 29.4 ± 4.6 μm ( P < .01). One hour after MCA occlusion, AGN-knockout mice exhibited a smaller ischemic core (defined as the region of ATP depletion) but a larger penumbra (the area of disturbed protein synthesis with preserved ATP). At 24 hours after MCA occlusion, this difference disappeared, and histologically visible lesions were of similar size in both strains. The observations show that in AGN-knockout mice the more efficient collateral blood supply delays ischemic injury despite the lower blood pressure. Pharmacologic suppression of angiotensin formation may prolong the therapeutic window for treatment of infarcts.

scholarly journals Novel Role of GPR35 (G-Protein–Coupled Receptor 35) in the Regulation of Endothelial Cell Function and Blood Pressure

Hypertension ◽  
2021 ◽  
Author(s):  
Hainan Li ◽  
Huong Nguyen ◽  
Sai Pranathi Meda Venkata ◽  
Jia Yi Koh ◽  
Anjaneyulu Kowluru ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endothelial Cell ◽  
G Protein ◽  
Arterial Blood Pressure ◽  
Knockout Mice ◽  
Wild Type ◽  
G Protein Coupled Receptor ◽  
Arterial Blood ◽  
G Protein Coupled ◽  
Wild Type Control

GPR35 (G-protein–coupled receptor 35) is a poorly characterized receptor that has garnered increased interest as a therapeutic target through its implications in a range of inflammatory and cardiovascular diseases, but its biological functions stay largely unknown. The current study evaluated the effect of GPR35 on endothelial cell (EC) functions and hemodynamic homeostasis. In primary human aortic ECs, the expression of GPR35 was manipulated by transfections of adenovirus carrying either GPR35 cDNA or shRNA against GPR35, using adenovirus carrying β-gal as control. Mouse aortic ECs were isolated and cultured from GPR35 knockout and wild-type control mice. Our results indicated that genetic inhibition of GPR35 in human and mouse ECs significantly promoted cell proliferation, migration, and tube formation in vitro. The GCH1 (guanosine triphosphate cyclohydrolase I)-mediated biosynthesis of tetrahydrobiopterin was enhanced, reducing intracellular superoxide. Knocking down GCH1 or eNOS (endothelial nitric oxide synthase) significantly blunted the robust angiogenesis induced by GPR35 suppression. Male GPR35 knockout mice demonstrated reduced basal arterial blood pressure and an attenuated onset of hypertension in deoxycorticosterone acetate-salt induced hypertensive model compared with male GPR35 wild-type control mice in vivo, with concomitant improved endothelium-dependent vasodilation and decreased superoxide in isolated aortas. The difference in arterial blood pressure was absent between female GPR35 wild-type control and female GPR35 knockout mice. Our study provides novel insights into the roles of GPR35 in endothelial function and vascular tone modulation that critically contribute to the pathophysiology of blood pressure elevation. Antagonizing GPR35 activity might represent a potentially effective therapeutic approach to restore EC function and hemodynamic homeostasis.

Inhibition of adenosine-1 receptor-mediated preglomerular vasoconstriction in AT1Areceptor-deficient mice

1998 ◽  
Vol 275 (6) ◽  
pp. F922-F927 ◽  
Author(s):  
Timothy Traynor ◽  
Tianxin Yang ◽  
Yuning G. Huang ◽  
Lois Arend ◽  
Michael I. Oliverio ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Knockout Mice ◽  
Vascular Reactivity ◽  
Feedback System ◽  
Tubuloglomerular Feedback ◽  
Arterial Blood ◽  
Simultaneous Activation ◽  
Arteriolar Tone

The effect of the adenosine type 1 receptor agonist N 6-cyclohexyladenosine (CHA) on glomerular vascular reactivity was studied in male angiotensin II type 1A (AT1A) receptor knockout mice (9). Vascular reactivity was assessed as the response of stop-flow pressure (PSF) to infusion of CHA into loops of Henle using micropuncture techniques. In AT1A +/+ mice at ambient arterial blood pressure (96.7 ± 2.8 mmHg), the presence of CHA (10−5 M) in the perfusate increased PSF responses from 6.8 ± 0.6 to 14.3 ± 0.9 mmHg when the loop of Henle of the index nephron was perfused and from 0.7 ± 0.3 to 12.3 ± 1.0 mmHg when the loop of an adjacent nephron was perfused. At reduced arterial blood pressure (82.8 ± 1.3 mmHg), index nephron perfusion with CHA increased PSF responses from 4.5 ± 0.3 to 9.4 ± 0.4 mmHg. In AT1A −/− mice with a mean arterial blood pressure of 80 ± 1.9 mmHg, CHA increased PSF responses only from 0.1 ± 0.3 to 3.6 ± 0.54 mmHg during index nephron perfusion and from 0.25 ± 0.2 to 2.7 ± 0.55 mmHg during adjacent nephron perfusion, significantly less than in wild-type animals ( P < 0.001). Responses to CHA were intermediate in AT1A +/− mice. Thus AT1A receptor knockout mice show a markedly reduced constrictor response to CHA both in the presence and absence of simultaneous activation of the tubuloglomerular feedback system. These data support the notion of a functional interaction between adenosine and angiotensin II in the regulation of afferent arteriolar tone.

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