Abstract
ACTH dependent and independent adrenocortical steroid hypertension in experimental animals is thought to be due to the 'mineralocorticoid' and/or 'glucocorticoid' activity of the steroid/s. Studies in sheep examining ACTH and adrenocortical steroid hypertension have provided evidence for a 'hypertensinogenic' class of steroid activity. A hypothesis is proposed to explain how the 'hypertensinogenic' actions of a steroid may produce hypertension. It is suggested that effects mediated via 'mineralocorticoid' and 'glucocorticoid' receptors may modulate or amplify the 'hypertensinogenic' activity. Individual steroids may express any, all or none of these three types of steroid hormone activity.
Published Version
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