Dopaminergic control of prolactin and blood pressure: altered control in essential hypertension.

This study examines the influence of dopamine on plasma catecholamine, prolactin (PRL), and mean arterial pressure (MAP) responses to upright posture and isometric handgrip exercise and the recumbent circadian PRL and MAP patterns in essential hypertension. Nine men with sustained essential hypertension and nine ageand weight-matched normotensive controls were studied after they had reached metabolic equilibrium on a constant intake of 100 mEq sodium and 80 mEq potassium. The hypertensive group, but not the normotensive group, displayed a PRL response to upright posture and isometric handgrip. Hypertensives and normotensives had similar basal supine catecholamine levels and similar epinephrine and dopamine responses to posture and handgrip. The hypertensives had greater (p < 0.01) norepinephrine (NE) responses to posture and handgrip than did the normotensives. Bromocriptine (BEC) depressed supine basal MAP in the hypertensives but not in the normotensives. BEC markedly decreased the basal PRL levels in both groups. BEC eliminated the PRL response to posture in the hypertensives and depressed the NE response to posture and handgrip to a greater extent (p < 0.01) in the hypertensives than in the normotensives. In the control period, a clear circadian rhythm of PRL and MAP was noted in both groups. In both groups an increase in PRL concentration occurred between 60 to 90 minutes after sleep onset, and was followed by several larger secretory episodes resulting in progressively higher levels during the night with peak values occurring at the end of the sleep period, generally at 0500 to 0600 hours. During the hour after awakening, a fall in PRL concentration began, and lowest levels were reached at approximately 1100 hours in both groups. The mean 24-hour PRL levels in the hypertensive group (12.6 ± 0.5 ng/ml) were higher (p < 0.01) than in the normotensives (10.8 ± 0.4 ng/ml). During the waking hours, there was a correlation (r = 0.57, p < 0.01) between recumbent PRL levels and MAP. BEC therapy lowered MAP levels throughout the 24 hours in the hypertensive group. BEC also eliminated the circadian rhythm of PRL secretion. Thus, circadian variations in PRL secretion and blood pressure appear to be modulated by a central and/or peripheral dopaminergic mechanism. Decreased dopaminergic activity in essential hypertension may account, in part, for aberrances in PRL secretion and elevated blood pressure in this disease state. (Hypertension 4: 431-438, 1982)