Effects of the Endothelin Receptor Blockade on Pressure-Natriuresis in Ercised and Sedentary SHR Female Rats

Location

CSU Ballroom

Start Date

18-4-2016 10:00 AM

End Date

18-4-2016 11:30 AM

Student's Major

Biological Sciences

Student's College

Science, Engineering and Technology

Mentor's Name

Penny Knoblich

Mentor's Department

Biological Sciences

Mentor's College

Science, Engineering and Technology

Description

This research was designed to investigate the mechanisms by which exercise affects blood pressure. Blood pressure is strongly influenced by blood volume, which is related to sodium (salt) and water retention by the kidneys. The kidneys excrete extra sodium and water when blood pressure is raised, a process called pressure natriuresis. Previous studies in this lab found that when female hypertensive rats (SHR) ercised, they excreted more sodium in their urine when blood pressure was raised, than did sedentary SHR. Ercise causes the blood vessels to secrete endothelin. Endothelin binds to two different receptors, the ETA and ETB receptors, which are found in the kidneys. The ETA receptors’ role is to constrict the blood vessels in the kidney, and increase sodium and water excretion. This research investigated the role of endothelin in the improvement in pressure natriuresis observed in exercised female SHR, by blocking the endothelin A (ETA) receptors. Twenty rats were randomly assigned to an exercise group (exercised voluntarily from 4 to 12 weeks of age) or a sedentary group. At 12 weeks of age, rats were anesthetized, and received either the ETA blocker or the vehicle control. After catheterization of the carotid artery and jugular vein, the rat was allowed a 30-minute equilibration period before the collection of a 15 minute baseline urine. Following this, arterial blood pressure was raised by ligating three abdominal arteries. Four additional urine samples were collected. Urine samples will be analyzed for sodium and water content, and values compared between groups.

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Apr 18th, 10:00 AM Apr 18th, 11:30 AM

Effects of the Endothelin Receptor Blockade on Pressure-Natriuresis in Ercised and Sedentary SHR Female Rats

CSU Ballroom

This research was designed to investigate the mechanisms by which exercise affects blood pressure. Blood pressure is strongly influenced by blood volume, which is related to sodium (salt) and water retention by the kidneys. The kidneys excrete extra sodium and water when blood pressure is raised, a process called pressure natriuresis. Previous studies in this lab found that when female hypertensive rats (SHR) ercised, they excreted more sodium in their urine when blood pressure was raised, than did sedentary SHR. Ercise causes the blood vessels to secrete endothelin. Endothelin binds to two different receptors, the ETA and ETB receptors, which are found in the kidneys. The ETA receptors’ role is to constrict the blood vessels in the kidney, and increase sodium and water excretion. This research investigated the role of endothelin in the improvement in pressure natriuresis observed in exercised female SHR, by blocking the endothelin A (ETA) receptors. Twenty rats were randomly assigned to an exercise group (exercised voluntarily from 4 to 12 weeks of age) or a sedentary group. At 12 weeks of age, rats were anesthetized, and received either the ETA blocker or the vehicle control. After catheterization of the carotid artery and jugular vein, the rat was allowed a 30-minute equilibration period before the collection of a 15 minute baseline urine. Following this, arterial blood pressure was raised by ligating three abdominal arteries. Four additional urine samples were collected. Urine samples will be analyzed for sodium and water content, and values compared between groups.

Recommended Citation

Quesada Olarte, Juan Jose and Okhumhekho Kassim. "Effects of the Endothelin Receptor Blockade on Pressure-Natriuresis in Ercised and Sedentary SHR Female Rats." Undergraduate Research Symposium, Mankato, MN, April 18, 2016.
https://cornerstone.lib.mnsu.edu/urs/2016/poster-session-A/20