Abstract:The presynaptic regulation of amino acid release from nerve terminals was investigated using synaptosomes prepared from the rat spinal cord. The basal releases of endogenous glutamate (Glu), aspartate (Asp), and y-aminobutyric acid (GABA) were 34.6, 21.5, and 10.0 pmol/min/ mg of protein, respectively. Exposure to a depolarizing concentration of KCl (30 mkI) evoked 2.7-, 1 . 5 , and 2.9-fold increases in Glu, Asp, and GABA release, respectively. Clonidine reduced the K+-evoked overflow of Glu to 56% of the control overflow with a potency (1C5J of 17 nM, but it did not affect K+-evoked overflow of Asp, GABA, and their basal releases. Similarly, noradrenaline inhibited the K' -evoked overflow of Glu, although phenylephrine and isoproterenol showed no effect. The inhibitory effect of clonidine was counteracted by a,-adrenoceptor antagonists, rauwolscine, yohimbine, and idazoxan, regardless of the imidazoline structures. Because Glu is considered a neurotransmitter of primary afferents that transmit both nociceptive and nonnociceptive stimuli in the spinal cord, these data suggest that part of Glu release may be regulated by the noradrenergic system through a2 adrenoceptors localized on the primary afferent terminals. The primary afferents that transmit peripheral signals to the second-order neurons in the spinal cord are differentiated by the diameters of the nerve fibers, corresponding to the conducting information. For example, pain is mediated by nociceptive nerves (A6

Two patients with primary hyperparathyroidism had hyperuricemia due to the decrease in urate clearance. In analysis by 4-component model system, the tubular secretion of urate commonly decreased without changes in either filtered urate or presecretory reabsorption of urate. Both patients had a reduction of urea clearance, and both parathyroidectomy in the former case and intravenous infusion of saline in the latter case could reduce the serum urate level associated with the increase in the ratio of urate clearance to creatinine clearance. It is of interest that the former case with a higher serum urate level had a relatively higher postsecretory reabsorption, even with the decrease in tubular secretion of urate. However, the latter patient with a lower serum urate level had a decrease in postsecretory reabsorption of urate in pro portion to the decrease in tubular secretion. These results suggest that in hyperuricemia patients with primary hyperparathyroidism, the reduction of tubular urate secretion via hypoperfusion of the capillary network is typically present, however, the severity of the hyperuricemia might be dependent on the dysfunction of the postsecretory reabsorption of urate. (Internal Medicine 31: 807-811, 1992)

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We conclude that hyperinsulinaemia may be involved in an increase in blood pressure in active acromegalics.

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