Radiotelemetry transmitters (model TA11PA-C10; Data Sciences International, St Paul, MN) were implanted in 12-week old mice, as detailed in the online-only Data Supplement and per our previous studies (n=12 WT, n=15 KO).9 (link), 10 (link) Systolic (SAP), diastolic (DAP) and mean arterial blood pressure (MAP), heart rate (HR) and locomotor activity were measured in conscious, unrestrained mice from 10-days after surgery for a period of 48 hours. To further determine the contribution of the RAS versus the sympathetic nervous system (SNS), we also measured cardiovascular parameters for 30-minutes following administration of pentolinium (5mg/kg; Sigma-Aldrich) to mice pre-treated with enalaprilat (an angiotensin converting enzyme, ACE, inhibitor, at 1mg/kg; Merck & Co.) during the active (dark) and inactive (light) period as previously described.6 (link) Sample size and power calculations were conducted prior to the study. These indicated that for an effect size d=1.67, we would need at least 11 mice per group to detect a difference of 5 mmHg in BP (power=0.95 and α=0.05).
Pentolinium
Manufactured by Merck Group
Sourced in Australia, United States
Pentolinium is a laboratory equipment product manufactured by Merck Group. It is a chemical compound used in various scientific research and analysis applications. The core function of Pentolinium is to serve as a reagent or analytical tool, but a detailed description cannot be provided while maintaining an unbiased and factual approach.
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Lab products found in correlation
5 protocols using pentolinium
1
Radiotelemetry Recording of Cardiovascular Parameters in Mice
2
Pentolinium Effects on Stress Response
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Twenty four hours after responses to stress stimuli had been recorded, responses of MAP, HR and locomotor activity were recorded for 30 min prior to and 30 min after administration of the ganglionic blocker, pentolinium (5 mg/kg i.p.; n = 5–7; Sigma, Sydney, Australia). This test was performed during the active phase of the circadian rhythm. Seventy two hours after pentolinium administration, mice were humanely killed by overdose with pentobarbitone (163 mg/kg).
3
Telemetric Monitoring of Cardiovascular Function in Mice
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Radiotelemetry transmitters (model TA11PA-C10; Data Sciences International, St Paul, MN) were implanted in 12-week old mice, as detailed in the online-only Data Supplement and per our previous studies (n=12 WT, n=15 KO). 9 Systolic (SAP), diastolic (DAP) and mean arterial blood pressure (MAP), heart rate (HR) and locomotor activity were measured in conscious, unrestrained mice from 10-days after surgery for a period of 48-hours. To further determine the contribution of the RAS versus the sympathetic nervous system (SNS), we also measured cardiovascular parameters for 30-minutes following administration of pentolinium (5mg/kg; Sigma-Aldrich) to mice pre-treated with enalaprilat (an angiotensin converting enzyme, ACE, inhibitor, at 1mg/kg; Merck & Co.) during the active (dark) and inactive (light) period as previously described. 7
4
Cardiovascular Responses to RAS Modulation
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Following a 30 min baseline recording, mice were administered the ACE inhibitor enalaprilat (1 mg/kg intraperitoneal; Merck & Co, Keniworth, NJ, USA), followed 40 minutes later by the ganglion blocker, pentolinium (5 mg/kg, intraperitoneal; Sigma-Aldrich, Castle Hill, NSW Australia) as described previously.3 ACE inhibition prior to ganglion blockade has been shown to reduce the compensatory response of the RAS following ganglion blockade, unmasking the full contribution of the SNS in BPH/2J mice. 4 The cardiovascular responses were evaluated during both the light (inactive) period and the dark (active) period, on separate days, two weeks after RD surgery.
5
Modulating Autonomic Cardiovascular Responses
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BPN/3J (n=3-5) and BPH/2J mice (n=3-5) were administered a ganglion blocker, pentolinium (5 mg/kg, IP; Sigma-Aldrich), 30 minutes after administration of the angiotensin-converting enzyme inhibitor, enalaprilat (1.5 mg/kg, IP; Merck & Co), as described previously. 3 (link) The cardiovascular responses to these drugs were measured during the dark period in mice 6 hours after an injection of almorexant (100 mg/kg, IP) and in untreated mice.
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