A B S T R A C T A possible role for dopamine in phosphate handling by the dog kidney was investigated by intrarenal artery infusions of dopamine. Dopamine increased fractional phosphate excretion both in the presence and absence of control of parathyroid hormone and calcitonin. In addition, dopamine increased both renal blood flow and sodium excretion; however, the phosphaturia was independent of these changes; since 30 min after completion of dopamine infusion, renal blood flow and sodium excretion returned to control levels and phosphate excretion remained elevated. For comparison, the vasodilator isoproterenol increased renal blood flow and sodium excretion without a significant change in fractional phosphate excretion. Thus, the phosphaturic effect of dopamine is probably independent of its vasodilator effect. The phosphaturic effect of dopamine could not be accounted for by subsequent conversion to norepinephrine, since norepinephrine was antiphosphaturic in the dog.The effect of endogenous dopamine on renal phosphate excretion was investigated by intrarenal infusion of the precursor dopa. Dopa was phosphaturic both in the presence and absence of parathyroid hormone and calcitonin. In dogs pretreated with carbidopa, which blocks conversion of dopa to dopamine, dopa was no longer phosphaturic, although the kidney remained responsive to dopamine. It is postulated that dopamine may play a role in the intrarenal regulation of phosphate excretion.

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Abstract• Our earlier studies revealed a weak alpha-adrenergic and beta-adrenergic activity of the cerebral vessels of the isolated perfused dog brain. The present investigations were undertaken to determine whether vascular adjustments occur in the cerebral circulation during longer periods of catecholamine infusions. The experiments were performed on six isolated canine brains cross perfused from donor dogs. Norepinephrine (2 /*g per minute), epinephrine (2 fig per minute), and isoprenaline (0.2 ng per minute) were applied intra-arterially (i.a.) for a period of ten minutes. Total venous outflow, perfusion pressure in the circle of Willis, and venous O 2 saturation were monitored continuously. Cerebral vascular resistance (CVR) and cerebral O 2 consumption (CMRO 2 ) were calculated. Based on the pressure-flow relationship tested in each brain, the indirect effects of catecholamines on CVR caused by autoregulatory influences were calculated and eliminated. During norepinephrine and epinephrine infusions cerebral blood flow (CBF) was found to be decreased by 10.2 ± 6.0% and 4.1 ± 3.3%, respectively, whereas during isoprenaline infusion CBF increased by 9.3 ± 3.6% (mean values ± SD). The maximal changes of CBF were reached in the first or second minute of catecholamine infusion and persisted up to the end of infusion (P > 0.05). After elimination of the indirect effects of catecholamines on CVR, the direct effects on CVR were reduced to about 50% of the original values and remained constant at the level reached during the whole period of infusion. CMRO 2 was not changed (P > 0.05) during infusion of the different catecholamines. Based on these investigations it is assumed that no pronounced vascular adjustments occur in the cerebral circulation during catecholamine infusions.

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