Long-Term Effects of Betamethasone on Blood Pressure and Hypothalamo-Pituitary-Adrenocortical Function in Spontaneously Hypertensive and Normotensive Rats

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Abstract
An enhanced hypothalamo-piutitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure is spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 wk of age, the rats were treated with 0.1 and 0.5 .mu.g betamethasone/ml drinking water for 7 wk. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 = 3.9 (mean .+-. standard error of the mean) to 203.1 .+-. 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 .+-. 4.0 mm Hg in response to 0.5 .mu.g betamethasone/ml drinking water. In WKY, blood pressure increased from 134.4 .+-. 3.3-148.2 .+-. 3.0 and 157.9 .+-. 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 .+-. 2.1 to 136.3 .+-. 3.2 and 135.6 .+-. 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all 3 strains. Stress-induced secretion of ACTH was markedly reduced by 0.5 .mu.g betamethasone/ml in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.

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