No abstract

The influence of dietary sodium chloride on the urinary excretion of prostaglandins (PGs) was studied in unanesthetized female rabbits housed in metabolic cages. Urinary PG levels were determined by radioimmunoassay, bioassay and gas chromatography-mass spectrometry. In the first experiment rabbits were fed at high (2.5%) and later a low (0.25%) sodium chloride diet ad libitum. A 2--5 fold increase in excretion of immunoreactive PGF2alpha (iPGF2alpha) and iPGE2 was noticed when animals were given the low salt diet. Since it could not be excluded that dietary factors other than sodium chloride contributed to the changes a second, more controlled experiment was undertaken. Rabbits were fed 30 g/kg per day of diets offering only in the content of sodium chloride, 2% and 0.37% respectively. On the high salt diet the rabbits excreted 0.1 +/- 0.04 microgram/day of PGE2 and 2.0 +/- 0.5 microgram/day of iPGF2alpha. After equilibration on the low salt diet the PGE2 excretion rate increased to 1.5 +/- 0.3 microgram/day (p less than 0.001) and that of iPGF2alpha to 3.4 +/- 0.4 microgram/day (p less than 0.01). These results thus point to an inverse relationship between renal sodium excretion and the activity of the renal prostaglandin system.

No abstract

The interrelations between angiotensin and catecholamine uptake have been studied in rats. Angiotensin was infused for either 5, 30, or 120 minutes at three dose levels: 1, 12, and 45 ng/kg/min. With short exposures to angiotensin, effects were seen in kidney, uterus, and adrenal gland. These organs had been previously shown to bind the greatest amount of tritiated peptide administered intravenously. In the 5-and 30-minute experiments angiotensin inhibited uptake of either metaraminol or norepinephrine in most tissues, especially at the higher dose levels, with the exception of the adrenal gland where uptake was increased. After the two-hour infusion inhibition of uptake was seen in most organs. When high titer angiotensin II antibodies were administered intravenously, responses to iv angiotensin were abolished. At this stage the uptake of tritiated norepinephrine was increased in kidney, heart, spleen, and vas deferens, while it was decreased in the adrenal gland. To see whether these biochemical findings are related to a physiological role, contractile responses of isolated perfused arteries of rabbits were studied. Angiotensin potentiated the increase in perfusion pressure after the infusion of norepinephrine, while angiotensin II antibodies decreased this response. Thus, it is concluded that angiotensin can modify the uptake and, hence, the inactivation of the sympathetic neurotransmitter and possibly by this mechanism alter the physiological response to norepinephrine and sympathetic stimulation.KEY WORDS norepinephrine uptake blood vessel reactivity angiotensin metaraminol uptake angiotensin antibodies rabbit isolated arteries 11-96