Induced Natriuresis on Spontaneously Hypertensive Female Rats

Location

CSU Ballroom

Start Date

11-4-2017 10:00 AM

End Date

11-4-2017 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

St Hypertension (high-blood pressure) can lead to several health issues. Blood pressure is strongly influenced by blood volume, which is related to sodium and water retention by the kidneys. The kidneys excrete extra sodium and water when blood pressure is raised, a process called pressure natriuresis. Regular exercise reduces blood pressure and stimulates the release of a chemical called endothelin (ET). Endothelin has three forms and it binds to two different receptors, ETA and ETB, both found in the kidneys. Elimination of the ET-1 receptors in the kidney-collecting duct prevents the normal pressure natriuresis response. Prior studies in this laboratory found that exercised female Spontaneously Hypertensive Rats (SHR) exhibited an increase in pressure natriuresis and had a greater number of endothelin receptors in the kidneys. Further understanding of exercise, endothelin, pressure natriuresis, and blood pressure could lead to better treatments for hypertension. Investigation of the role of endothelin in the exercise-induced improvement in pressure natriuresis was carried using an ETA receptor blocker. Female SHRs were assigned to an exercised group, which ran voluntarily from 4 to 12 weeks of age, or a sedentary group. At 12 weeks of age, the rats were anesthetized and given either the ETA blocker or the vehicle control. After catheterization of the carotid artery and jugular vein, a baseline urine sample was collected. Afterwards, arterial blood pressure was raised by ligating three abdominal arteries. Four additional urine samples were collected at the higher blood pressure, analyzed for sodium and water content, and compared between groups.

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

Induced Natriuresis on Spontaneously Hypertensive Female Rats

CSU Ballroom

St Hypertension (high-blood pressure) can lead to several health issues. Blood pressure is strongly influenced by blood volume, which is related to sodium and water retention by the kidneys. The kidneys excrete extra sodium and water when blood pressure is raised, a process called pressure natriuresis. Regular exercise reduces blood pressure and stimulates the release of a chemical called endothelin (ET). Endothelin has three forms and it binds to two different receptors, ETA and ETB, both found in the kidneys. Elimination of the ET-1 receptors in the kidney-collecting duct prevents the normal pressure natriuresis response. Prior studies in this laboratory found that exercised female Spontaneously Hypertensive Rats (SHR) exhibited an increase in pressure natriuresis and had a greater number of endothelin receptors in the kidneys. Further understanding of exercise, endothelin, pressure natriuresis, and blood pressure could lead to better treatments for hypertension. Investigation of the role of endothelin in the exercise-induced improvement in pressure natriuresis was carried using an ETA receptor blocker. Female SHRs were assigned to an exercised group, which ran voluntarily from 4 to 12 weeks of age, or a sedentary group. At 12 weeks of age, the rats were anesthetized and given either the ETA blocker or the vehicle control. After catheterization of the carotid artery and jugular vein, a baseline urine sample was collected. Afterwards, arterial blood pressure was raised by ligating three abdominal arteries. Four additional urine samples were collected at the higher blood pressure, analyzed for sodium and water content, and compared between groups.

Recommended Citation

Kassim, Okhumhekho and Jill Knepprath. "Induced Natriuresis on Spontaneously Hypertensive Female Rats." Undergraduate Research Symposium, Mankato, MN, April 11, 2017.
https://cornerstone.lib.mnsu.edu/urs/2017/poster-session-A/15