Following an intravenous loading injection of 75 U.S.P. Units of Para-Thor-Mone (Eli Lilly and Co.), seven conscious, non-pregnant, non-lactating Merino ewes were infused with a maintenance dose of the hormone at a rate of 4'75 U.S.P. units/min for 2 hr. The classical hypercalcaemia and hypophosphataemia of the non-ruminant was observed, but the hypercalcaemia was only small. Plasma potassium concentration decreased, while there were no changes in plasma sodium, chloride or magnesium. The classical phosphaturic effect of the hormone was not observed, only trace amounts of phosphate being excreted throughout the experiment. Urinary excretion of calcium and magnesium decreased, urine flow and urinary excretion of sodium, potassium, chloride, bicarbonate and urine pH increased. Glomerular filtration rate was unaffected, but renal plasma flow increased. The concentration and secretion rate of salivary phosphate increased markedly. Changes in the other important salivary electrolytes (sodium, potassium, chloride, bicarbonate and hydrogen ion) also occurred, but it was difficult to separate primary from secondary effects of the hormnone. Saliva flow rate increased transiently following hormone injection, but the effect was not sustained by the maintenance infusion.Although the kidney is the major site of phosphorus regulation in nonruminants [Pitts and Alexander, 1944], the salivary glands appear to be of paramount importance in sheep [Compere, 1966; Clark, Budtz-Olsen, Cross, Bauert and Finnamore, 1973;Tomas and Somers, 1974] and probably all ruminants under normal dietary conditions. It therefore becomes desirable to establish the effects of parathyroid hormone in this species, and particularly to clarify any interaction of the hormone with the salivary glands.The information presently available on the effects of parathyroid hormone in sheep is incomplete and inconsistent. In the experiments of Lotz, Talmage and Comar [1954] and Alexander and Nixon [1969] on adult sheep, the classical pronounced phosphaturia of the non-ruminant was virtually absent. In contrast foetal sheep exhibit a pronounced phosphaturia when infused with the hormone [Alexander and Nixon, 1969;Smith, Tinglof, Meuli and Borden, 1969], and Barlet and Care [1972] observed it to cause a significant increase in urinary phosphate excretion in two months old lambs fed a diet of hay and concentrates. A possible effect of the hormone on the salivary glands of ruminants does not appear to have been examined.The object of the present work was to determine the acute effects of intravenous infusion of parathyroid hormone on various urinary, plasma and salivary parameters in normal adult sheep.

The excretion of electrolytes was measured during infusion of isosmotic NaCl and hyperosmotic NaCl, KCl, KHCO3 and KH2PO4. The increases in G.F.R., urine flow and urinary excretion of potassium, sodium, chloride, bicarbonate and solute during the infusion ofpotassium saltswere significantly greaterthan those duringthe isosmotic and hyperosmotic NaCl infusions; this finding excludes the rate of infusion and hyperosmolality of infusate as major contributors in the response to potassium infusion. The renal clearance ofpotassium was significantly higher in the sheep receiving the bicarbonate salt than in the animals receiving the chloride or the phosphate salts. Potassium bicarbonate loading was associated with low chloride excretion and potassium phosphate loading with low bicarbonate excretion. Potassium loading resulted in high rates of bicarbonate excretion in some experiments, which indicates a reduction in solute reabsorption in the proximal tubule. During the potassium infusions, the urinary calcium excretion rate and urinary pH were inversely correlated, renal magnesium excretion was not altered significantly and phosphate excretion was increased only when phosphate was infused. Salivary potassium secretion was highest in the phosphate-loaded sheep and potassium retention was lowest in the sheep receiving KCI infusions.Both oral and parenteral loading with potassium salts have been shown to increase the renal excretion of water, potassium, sodium, chloride and bicarbonate in a number of mammalian species including man, but the magnitudes of these effects vary considerably [Bassett, Elden and McCann, 1932;Keith and Binger, 1935;Laragh, 1954;Laragh and Capeci, 1955; Kahn and Bohrer, 1967]. The effect of potassium loading on the renal excretion of calcium, magnesium and phosphate ions has rarely been examined and the data available frequently conflict [Miller, 1926;Bassett et al., 1932;Winkler and Smith, 1942].This variability of the responses to potassium administration may be due to differences in the experimental design. The main areas of difference are the routes of administration, rates of infusion, solution osmolalities, potassium salts used and the mineral and hormonal status of the experimental animals.In this study an attempt has been made to separate the effects of potassium loading on urine formation and composition from the effects attributable to the rate of fluid infusion, the solution osmolality and the species of potassium salt. The potassium salts compared were chloride, bicarbonate and phosphate, these being the salts most frequently studied in the past.Since the high rate of production of saliva in the sheep could provide an alternative site for sequestration of potassium during potassium loading, parotid saliva was collected to give a measure of salivary potassium secretion.

SUMMARY The acute effects of vasopressin (40 mU) were studied in the conscious sheep. Vasopressin caused consistent increases in K and C1 excretion and variable increases in Na and total solute output. These changes occurred within 10 min., reached a peak within 30 min. and subsided within 60 min. When the urine was initially dilute (< 800 μosmoles/ml.) vasopressin caused an antidiuresis. When the original concentration exceeded 1000 (μosmoles/ml. vasopressin caused small increases in urine flow. Vasopressin always increased water reabsorption relative to solute reabsorption.

SUMMARYSaralasin, an angiotensin II analogue and receptor blocker, was infused at 7 and 15 ,ug. min-' into dehydrated conscious Merino ewes. This caused mean arterial blood pressure, cardiac output, heart rate and renal vascular resistance to fall, and central venous pressure to rise. Renal plasma flow was unaffected but there were significant reductions in glomerular filtration rate, filtration fraction, urine flow, sodium and potassium excretion, solute clearance and solute-free water reabsorption. It is suggested that saralasin produced these effects by inhibiting endogenQus angiotensin II activity, and in particular by causing a reduction in renal post-glomerular resistance. This in turn caused a fall in glomerular filtration rate and filtration fraction. While saralasin might have had effects on renal tubular function and perhaps on vasopressin secretion, the observed effects on renal function can be explained by the decrease in glomerular filtration rate and filtration fraction.

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