Effect of estrogen on cardiac and vascular adrenergic receptors in the spontaneously hypertensive rat (SHR) / by George S. Fleming.
| Author/creator | Fleming, George S. author. |
| Other author | Iams, Samuel G., degree supervisor. |
| Other author | Scemama, Jean-Luc, degree supervisor. |
| Other author | East Carolina University. Department of Biology. |
| Format | Theses and dissertations |
| Production | 1999. |
| Description | vii, 84 leaves : illustrations ; 28 cm |
| Supplemental Content | Access via ScholarShip |
| Subjects |
| Summary | Results from clinical trials suggest that the female reproductive hormones, particularly estrogen, may play a protective role against the development of cardiovascular disease (CVD), including hypertension, in women. Such an assumption is based upon evidence from studies showing that premenopausal women have approximately 20% the CVD mortality when compared to men, whereas postmenopausal women have approximately the same CVD mortality as age matched men. Such results have also been obtained in premenopausal women which have undergone surgical ovariectomy. Administration of exogenous estrogens attenuates the development of CVD, with the risk of CVD mortality in treated females being similar to premenopausal women. While the mechanism of estrogen's actions are unclear, it has been suggested that estrogen may alter populations of cell surface receptors known as adrenergic receptors. Female normotensive Wistar-Kyoto and Spontaneously Hypertensive Rats (SHRs) were used to determine if a,) estrogen treatment would prevent the development of hypertension, b,) alterations in cardiac and/or vascular adrenergic receptors are associated with the pathogenesis of hypertension, and c,) estrogen treatment leads to alterations in cardiac or vascular adrenoceptor populations. Systolic blood pressures were significantly higher in SHR controls than in WKY controls. Estrogen treatment induced a significant decrease in systolic blood pressures in the SHRs. Ventricular alpha-1 adrenergic receptor densities were similar in all groups with the exception of the SHR treatment group, which was higher (though not statistically significant). The total density of the alpha-1 a receptor subtype was also increased by estrogen treatment in the SHR. Total ventricular alpha-2 adrenergic receptor populations were essentially unchanged between WKY and SHR controls or with estrogen treatment. Total beta adrenergic receptors were unchanged in SHR controls when compared to WKY controls. In the rat tail artery, both alpha-1 and alpha-la density was significantly higher in SHR controls than in WKY controls. Estrogen treatment significantly lowered alpha-1 and alpha-la densities in both WKYs and SHRs. It is possible that alterations in adrenergic receptor populations may be one of the mechanisms through which estrogen exerts its hypotensive effects. |
| General note | Submitted to the faculty of the Department of Biology. |
| General note | Advisor: Samuel G. lams |
| General note | Advisor: Jean-Luc Scemama |
| Dissertation note | M.S. East Carolina University 1999 |
| Bibliography note | Includes bibliographical references (leaves 76-84). |
| Genre/form | Academic theses. |
| Genre/form | Academic theses. |
| Genre/form | Thèses et écrits académiques. |
Availability
| Library | Location | Call Number | Status | Item Actions |
|---|---|---|---|---|
| Joyner | University Archives | ASK AT SPECIAL COLLECTIONS DESK | ✔ Available | Request Material |
| Electronic Resources | ✔ Available |