Neurocirculatory Regulation in Cortisol-Induced Hypertension

Effects of chronic glucocorticoid treatment on arterial baroreflex function and on cardiac beta- and vascular alpha-adrenoceptor-mediated responses were assessed in conscious, unrestrained Wistar-Kyoto rats. Cortisol (25 mg/kg/day) was administered for seven days using a subcutaneous reservoir pump. Arterial baroreflex-cardiac sensitivity was assessed by examining the relationship of the cardiac interbeat interval to the mean arterial blood pressure during phenylephrine or nitroprusside challenge; baroreflex-sympathoneural sensitivity was assessed from the ratio of the increase in the arterial norepinephrine concentration to the decrease in mean arterial pressure at 15 min during intravenous infusion of nitroprusside; cardiac beta-adrenoceptor-mediated responsiveness was estimated from heart rate responses to bolus-injected isoproterenol; and vascular alpha-adrenoceptor-mediated responsiveness was estimated from peak mean arterial pressure responses to bolus-injected phenylephrine. Cortisol treatment increased mean arterial pressure, decreased heart rate, and increased heart rate responses to isoproterenol, whereas baroreflex-vagal sensitivity, baroreflex-sympathoneural sensitivity, and pressor responses to phenylephrine were unaffected. The results indicate that hypertension due to chronic cortisol administration is not associated with decreased sensitivity of the baroreceptor-cardiac reflex. Baroreflex-sympathoneural sensitivity and alpha 1-adrenoceptor responsiveness also remain normal, whereas beta-adrenoceptor responsiveness is increased. The findings suggest that the pattern of neurocirculatory adjustment in glucocorticoid hypertension differs from that seen in other forms of hypertension.