The Effect of Reduced Aldosterone Levels on the Development of Hypertension in the Spontaneously Hypertensive Rat (SHR)
Location
CSU 285
Start Date
25-4-2005 10:30 AM
End Date
25-4-2005 12:00 PM
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
Hypertension, or high blood pressure, is a common disorder. The underlying cause of hypertension is, as yet, unidentified. Many researchers believe an expansion of blood volume precedes the rise in blood pressure. Aldosterone, an important regulator of blood volume, is produced in the outermost layer of the adrenal cortex. Aldosterone promotes the reabsorption of sodium ions (Na+) from kidney tubules back into the blood. Since water is reabsorbed with sodium, aldosterone increases blood volume and blood pressure. The role of aldosterone in hypertension has been studied using receptor blocking agents, or complete adrenalectomy, (removal of both adrenal glands), with each method resulting in confounding variables. A surgically-induced low-aldosterone state has been developed in this laboratory. The process involves removal of one adrenal gland, and cryo-destruction of the outer layer of the remaining gland. This procedure markedly reduces aldosterone levels, while maintaining the production of the other hormones of the adrenal gland. This study evaluates the effect of this treatment on the development of hypertension in a genetically hypertensive rat model, the spontaneously hypertensive rat (SHR). Blood pressure in the SHR begins to rise at 6 weeks of age and peaks at 16 weeks, making it an acceptable model for the study of hypertension. Methods: Four to six week old SHR were subjected to either sham surgery (identical opening and closing of the abdominal cavity), or the adrenalectomy and freezing procedure. Post-surgery, blood pressure, heart rate, and weight were measured bi-weekly until rats reached 4 months of age.
The Effect of Reduced Aldosterone Levels on the Development of Hypertension in the Spontaneously Hypertensive Rat (SHR)
CSU 285
Hypertension, or high blood pressure, is a common disorder. The underlying cause of hypertension is, as yet, unidentified. Many researchers believe an expansion of blood volume precedes the rise in blood pressure. Aldosterone, an important regulator of blood volume, is produced in the outermost layer of the adrenal cortex. Aldosterone promotes the reabsorption of sodium ions (Na+) from kidney tubules back into the blood. Since water is reabsorbed with sodium, aldosterone increases blood volume and blood pressure. The role of aldosterone in hypertension has been studied using receptor blocking agents, or complete adrenalectomy, (removal of both adrenal glands), with each method resulting in confounding variables. A surgically-induced low-aldosterone state has been developed in this laboratory. The process involves removal of one adrenal gland, and cryo-destruction of the outer layer of the remaining gland. This procedure markedly reduces aldosterone levels, while maintaining the production of the other hormones of the adrenal gland. This study evaluates the effect of this treatment on the development of hypertension in a genetically hypertensive rat model, the spontaneously hypertensive rat (SHR). Blood pressure in the SHR begins to rise at 6 weeks of age and peaks at 16 weeks, making it an acceptable model for the study of hypertension. Methods: Four to six week old SHR were subjected to either sham surgery (identical opening and closing of the abdominal cavity), or the adrenalectomy and freezing procedure. Post-surgery, blood pressure, heart rate, and weight were measured bi-weekly until rats reached 4 months of age.
Recommended Citation
Robinson, Richard. "The Effect of Reduced Aldosterone Levels on the Development of Hypertension in the Spontaneously Hypertensive Rat (SHR)." Undergraduate Research Symposium, Mankato, MN, April 25, 2005.
https://cornerstone.lib.mnsu.edu/urs/2005/oral-session-D/2
