Hemodynamics of dexamethasone-induced hypertension in the rat

Although dexamethasone (DEX) is known to cause hypertension in humans and in animals, the hemodynamic characteristics of DEX-induced hypertension (DEX-HT) in the rat remain unclear. This study evaluated central and regional hemodynamics, and the role of total peripheral resistance (TPR) using a vasodilator minoxidil. Rats were divided into four groups, namely saline ( n =20), DEX ( n =21), minoxidil+saline ( n =10) and minoxidil+DEX ( n =10). Tail-cuff systolic blood pressure was recorded every second day. After 10–14 days of treatment, central (saline: n =9, DEX: n =10) and regional (saline: n =11, DEX: n =11) hemodynamic parameters were measured. Central hemodynamic data were also obtained from minoxidil-treated rats. DEX increased blood pressure ( P <0.0005) in association with an increase in TPR ( P <0.05). However, individual assessments of renal, mesenteric and hindquarter circulations did not detect any significant increase in resistance in these beds. Minoxidil increased cardiac output ( P′ <0.01) and cardiac index ( P′ <0.005) as well as decreased TPR ( P′ <0.05) without affecting DEX-HT. DEX prevented weight gain and decreased thymus weight. The increase in TPR in DEX-HT in rats was not simply explained by isolated alterations to resistance in the renal, mesenteric or hindquarter circulations. Minoxidil effectively prevented the increase in TPR but not the increase in blood pressure, suggesting that an increase in TPR is not essential for DEX-induced blood pressure increase.