ang ii Search Results


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Alomone Labs angiotensin ii
A- Mice survival after hypertension onset (days after beginning of <t>Ang</t> <t>II</t> infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.
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Shanghai Korain Biotech Co Ltd ang ii
A- Mice survival after hypertension onset (days after beginning of <t>Ang</t> <t>II</t> infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.
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Proteintech anti human angiotensin
A- Mice survival after hypertension onset (days after beginning of <t>Ang</t> <t>II</t> infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.
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Novus Biologicals anti ang ii antibody
A- Mice survival after hypertension onset (days after beginning of <t>Ang</t> <t>II</t> infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.
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Cusabio ang ii csb e04494r elisa kits
Effects of Rb1 and Rg3 on blood pressure, CWI and RAS activity in the serum. (A) SBP, (B) DBP and (C) PP of rats prior to and following 6 weeks treatment. (D) Body and (E) heart weights and (F) CWI. Serum (G) ACE and (H) <t>Ang</t> <t>II</t> levels. Data are presented as the mean ± standard deviation, n=8 (A-F) or n=6 (G-H) for each group. *P<0.05 vs. WKY group prior to treatment; # P<0.05 vs. WKY group following treatment; $ P<0.05 vs. SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; CWI, cardiac weight index; RAS, renin angiotensin system; SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; ACE, angiotensin converting enzyme; Ang II, angiotensin II; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.
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Alomone Labs angiotensin iii
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
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Shanghai Korain Biotech Co Ltd leptin
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
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Boster Bio rabbit anti agt
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
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ALPCO ang ii
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
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Ubio Biotechnology Systems Pvt Ltd rat angiotensin ii (ang ii) enzyme-linked immunosorbent assay (elisa) kit
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
Rat Angiotensin Ii (Ang Ii) Enzyme Linked Immunosorbent Assay (Elisa) Kit, supplied by Ubio Biotechnology Systems Pvt Ltd, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Enzo Biochem plasma ang ii (angiotensin ii)
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
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Beijing Solarbio Science sodium pyruvate solution ang ii
ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of <t>ANG</t> <t>III</t> induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.
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Image Search Results


A- Mice survival after hypertension onset (days after beginning of Ang II infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: A- Mice survival after hypertension onset (days after beginning of Ang II infusion). N= 20 C57BL6/J (B6J) and 129Sv (129) B- Mean daytime telemetry blood pressure N= 4 B6J and 129Sv. Values represent mean ± SEM. C- Mean nighttime telemetry blood pressure. N= 4 B6J and 129Sv. Values represent mean ± SEM.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques:

A- In vivo imaging (microm) performed on 129Sv (129) and C57BL6/J (B6J) mice 8 days after angiotensin-2 pump implantation shows haemorrhage (arrows) and hard exudates (asterisks). Haemorrhagic spots are only found on the 129Sv eye fundus and density of hard exudates is increased in 129 mice compared to B6J mice. B-Haemorrhagic spots (arrow heads) in retinas at day 7 of hypertensive challenge and associated quantification. Values represent mean ± SEM of 5 mice per group. * p < 0.05. C- Subretinal swelling assessed by OCT at day 7 of hypertensive challenge and associated quantification. The white arrow shows retinal detachment. D- Retinal capillary density assessed at day 7 of hypertensive challenge. Representative images of the retina vascular network stained with lectin antibody. Values represent mean ± SEM of 4 B6J mice and 8 129 mice. *** p < 0.001.

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: A- In vivo imaging (microm) performed on 129Sv (129) and C57BL6/J (B6J) mice 8 days after angiotensin-2 pump implantation shows haemorrhage (arrows) and hard exudates (asterisks). Haemorrhagic spots are only found on the 129Sv eye fundus and density of hard exudates is increased in 129 mice compared to B6J mice. B-Haemorrhagic spots (arrow heads) in retinas at day 7 of hypertensive challenge and associated quantification. Values represent mean ± SEM of 5 mice per group. * p < 0.05. C- Subretinal swelling assessed by OCT at day 7 of hypertensive challenge and associated quantification. The white arrow shows retinal detachment. D- Retinal capillary density assessed at day 7 of hypertensive challenge. Representative images of the retina vascular network stained with lectin antibody. Values represent mean ± SEM of 4 B6J mice and 8 129 mice. *** p < 0.001.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques: In Vivo Imaging, Staining

Typical ECG changes seen in SV129 mice treated for 2 weeks with angiotensin II (n = 5-7 mice/group. A. episode of atrial flutter B. atrial fibrillation. C. ventricular ectopy seen in the Ang II group; D. short run of ventricular tachycardia; E. sustained ventricular tachycardia degenerating in ventricular fibrillation and cardiac death.

Journal: bioRxiv

Article Title: A novel mouse model of hypertensive emergency with multiorgan microvascular disease implicating the VEGFA/sFlt-1 balance

doi: 10.64898/2026.03.03.709451

Figure Lengend Snippet: Typical ECG changes seen in SV129 mice treated for 2 weeks with angiotensin II (n = 5-7 mice/group. A. episode of atrial flutter B. atrial fibrillation. C. ventricular ectopy seen in the Ang II group; D. short run of ventricular tachycardia; E. sustained ventricular tachycardia degenerating in ventricular fibrillation and cardiac death.

Article Snippet: The hypertensive model was induced by subcutaneous infusion of angiotensin II (Ang II) (Alomone, GPA-100) at 1 μg/kg/min for 7 or 14 days, via osmotic minipumps (Alzet, model 1007D or 1002) in 10- to 16-week-old males.

Techniques:

Effects of Rb1 and Rg3 on blood pressure, CWI and RAS activity in the serum. (A) SBP, (B) DBP and (C) PP of rats prior to and following 6 weeks treatment. (D) Body and (E) heart weights and (F) CWI. Serum (G) ACE and (H) Ang II levels. Data are presented as the mean ± standard deviation, n=8 (A-F) or n=6 (G-H) for each group. *P<0.05 vs. WKY group prior to treatment; # P<0.05 vs. WKY group following treatment; $ P<0.05 vs. SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; CWI, cardiac weight index; RAS, renin angiotensin system; SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; ACE, angiotensin converting enzyme; Ang II, angiotensin II; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Journal: Experimental and Therapeutic Medicine

Article Title: Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

doi: 10.3892/etm.2017.5198

Figure Lengend Snippet: Effects of Rb1 and Rg3 on blood pressure, CWI and RAS activity in the serum. (A) SBP, (B) DBP and (C) PP of rats prior to and following 6 weeks treatment. (D) Body and (E) heart weights and (F) CWI. Serum (G) ACE and (H) Ang II levels. Data are presented as the mean ± standard deviation, n=8 (A-F) or n=6 (G-H) for each group. *P<0.05 vs. WKY group prior to treatment; # P<0.05 vs. WKY group following treatment; $ P<0.05 vs. SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; CWI, cardiac weight index; RAS, renin angiotensin system; SBP, systolic blood pressure; DBP, diastolic blood pressure; PP, pulse pressure; ACE, angiotensin converting enzyme; Ang II, angiotensin II; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Article Snippet: ACE (CSB-E04490r) and Ang II (CSB-E04494r) ELISA kits were purchased from Cusabio Biotech Co., Ltd. (Wuhan, China) and the assays were completed by this company.

Techniques: Activity Assay, Standard Deviation

Effects of Rb1 and Rg3 on RAS and TGF-β1 levels in the myocardium. (A) Representative IHC staining photomicrographs of myocardium tissue. (Magnification, ×400). Antibodies against ACE, Ang II, AT1 and TGF-β1 were used as the primary antibodies. (B-E) Quantitative results of IHC staining, which were presented as IOD/Area and were proportional to the levels of ACE, Ang II, AT1 and TGF-β1. Data are presented as the mean ± standard deviation, n=4. # P<0.05 vs. the WKY group following treatment; $ P<0.05 vs. the SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; RAS, renin angiotensin system; TGF-β1, transforming growth factor β1; IHC, immunohistochemistry; ACE, angiotensin converting enzyme; Ang II, angiotensin II; AT1, Ang II receptor type 1; IOD, integrated optical density; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Journal: Experimental and Therapeutic Medicine

Article Title: Ginsenoside Rg3 induces ginsenoside Rb1-comparable cardioprotective effects independent of reducing blood pressure in spontaneously hypertensive rats

doi: 10.3892/etm.2017.5198

Figure Lengend Snippet: Effects of Rb1 and Rg3 on RAS and TGF-β1 levels in the myocardium. (A) Representative IHC staining photomicrographs of myocardium tissue. (Magnification, ×400). Antibodies against ACE, Ang II, AT1 and TGF-β1 were used as the primary antibodies. (B-E) Quantitative results of IHC staining, which were presented as IOD/Area and were proportional to the levels of ACE, Ang II, AT1 and TGF-β1. Data are presented as the mean ± standard deviation, n=4. # P<0.05 vs. the WKY group following treatment; $ P<0.05 vs. the SHR group following treatment. Rb1, ginsenoside Rb1; Rg3, ginsenoside Rg3; RAS, renin angiotensin system; TGF-β1, transforming growth factor β1; IHC, immunohistochemistry; ACE, angiotensin converting enzyme; Ang II, angiotensin II; AT1, Ang II receptor type 1; IOD, integrated optical density; WKY, Wistar-Kyoto; SHR, spontaneously hypertensive rats.

Article Snippet: ACE (CSB-E04490r) and Ang II (CSB-E04494r) ELISA kits were purchased from Cusabio Biotech Co., Ltd. (Wuhan, China) and the assays were completed by this company.

Techniques: Immunohistochemistry, Standard Deviation

ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG III induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.

Journal: Scientific Reports

Article Title: Sniffer cells for the detection of neural Angiotensin II in vitro

doi: 10.1038/s41598-019-45262-4

Figure Lengend Snippet: ANG II mediated increases in sniffer cell fluorescence. ( A ) ANG II (100 nM) induced a robust but transient increase in GCaMP fluorescence that was blocked by the AT1aR receptor antagonist Losartan (10 µM). Control n = 39, Losartan n = 38. ( B ) Data shows that bath application of glutamate (50 µM), GABA (50 µM), and carbachol (50 µM) failed to change fluorescent intensity of sniffer cells transfected with GCaMP (n = 29) or GCaMP + AT1aR (n = 38). ANG II (100 nM) did increase fluorescent intensity of sniffer cells, but only in sniffer cells transfected with GCaMP + AT1aR. Dose-dependent effects of ANG II and related compounds were also measured. ( C ) GCaMP + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (100 nM, n = 10). ( D ) Bath application of ANG III induced a dose-dependent increase in GCaMP + AT1aR sniffer cell fluorescence. Bath application of ANG (1–7) or bradykinin did not induce a change in GCaMP + AT1aR sniffer cell fluorescence at any of the doses tested (0.1–100 nM, n = 17–41). ( E ) R-GECO + AT1aR sniffer cells exhibit dose-dependent increases in fluorescence in response to bath application of ANG II (n = 17). R-GECO only cells did not respond to ANG II (n = 27). ( F ) ANG II-mediated increases in R-GECO + AT1aR are blocked by bath application of Losartan (10 µM, n = 17). *p < 0.05, **p < 0.01.

Article Snippet: Carbachol (50 μM), Angiotensin 1–7 (0.1–100 nM), Bradykinin (0.1–100 nM), and Losartan (10 μM) were purchased from Tocris (Minneapolis, MN) and Angiotensin III (0.1–100 nM) was purchased from Alomone Labs (Jerusalem, Israel).

Techniques: Fluorescence, Control, Transfection