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SUMMARY The uptake and content of serotonin in blood platelets were studied in patients with essential hypertension and in five families in which at least one member was hypertensive. Blood was obtained from male and female normotensive volunteers and hypertensive patients who were free of medication. Lineweaver-Burk plots of 3 H-serotonin uptake from both control subjects and hypertensive patients were linear, which suggested simple Michaelis-Menten uptake kinetics. The maximal uptake velocity (Vmax) in hypertensive patients was significantly lower than in control subjects T HERE is increasing experimental evidence relating serotonin and blood pressure regulation. In the peripheral vessels, the vasoconstrictor effects of serotonin result in increased vascular resistance. In addition, serotonin can also accentuate the vasoconstricting effects of other substances.' Serotonin is present in the heart and blood vessels.2 Blockade of serotonergic receptors in these structures by ketanserin antagonizes the vasoconstricting effects of serotonin and reduces blood pressure in hypertensive animals and humans.1 In the central nervous system, the role of serotonin in regulating the blood pressure is less clear. Although serotonergic neurons are located in areas of the brain involved in cardiovascular regulation, 3 pharmacological manipulation of these brain areas by either direct injections of serotonin 4 5 or by intravenous injections of serotonergic agonists, antagonists, and inhibitors of synthesis 6 " 10 has demonstrated that serotonergic neurons can both inhibit and facilitate central sympathetic activity.

CSF was removed at a constant flow rate of 1 microliter/min from the third ventricle of anesthetized rats. Five microliter CSF samples were directly injected every 15 min into a liquid chromatographic system coupled with an amperometric detector. Mean CSF values for free dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA) were 1.4, 0.9, and 2.6 X 10(-6)M respectively. High doses of probenecid resulted in a linear increase of acidic metabolite concentrations which gave an index of the fractional turnover rates related to the resorption by the weak organic acid carrier. Accumulation rates were 0.24, 0.87, and 1.58 mumol/l/h for DOPAC, HVA and 5-HIAA respectively. This route of elimination was predominant for 5-HIAA while it represented only a small part of total turnover for DOPAC. A high elimination rate constant for HVA validates the use of control levels of this metabolite as an indication of fractional HVA turnover dependent upon probenecid-sensitive carrier.

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