Hyperprolactinaemia in the spontaneously hypertensive rat.
A hypothalamic role in the aetiology of hypertension in the spontaneously hypertensive rat (SHR) has been suggested by prior observations. In an attempt to determine whether the central control of prolactin (PRL) release is altered in the SHR we have compared the PRL response to immobilization stress, thyrotrophin releasing hormone (TRH), haloperidol, and L-DOPA in the SHR and in normotensive Wistar control rats. Carotid artery catheters were inserted 48 h prior to the PRL response studies and the catheters were maintained patent with heparinized saline. Timed blood samples were obtained in SHR and control rats weighing 180-225 g. The SHR demonstrated elevated basal serum levels of PRL and greater PRL responses to stress. However, administration of L-DOPA resulted in a similar suppression of serum PRL in the SHR and in the normotensive controls. These findings suggest alteration in the central control of PRL release in the SHR. Observations of elevated basal PRL, exaggerated PRL in response to L-DOPA in SHR are consistent with normal pituitary responsiveness to dopamine suppression of PRL release, but defective hypothalamic metabolism of dopamine. Alterations in central dopamine control mechanisms in the SHR may play a role in the pathogenesis of essential hypertension in these animals.
D000818:Animals; D006220:Haloperidol; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D007031:Hypothalamus / Q000503:physiopathology; D007103:Immobilization; D007980:Levodopa; D008297:Male; D011388:Prolactin / Q000097:blood* / Q000378:metabolism; D051381:Rats; D013312:Stress, Physiological; D013973:Thyrotropin-Releasing Hormone
D007980:Levodopa; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D006220:Haloperidol