An increase of the intrarenal pressure to 40 mmHg induced by ureteral constriction or by kidney compression is shown to be followed by increased renal blood flow in anesthetized dogs. This hyperemia is probably the result of enhanced intrarenal prostaglandin activity since it is followed by increased urinary prostaglandin E excretion and is abolished by indomethacin pretreatment. The increase of renal blood flow seems to be due to dilation of the afferent arteriole in order to maintain the filtration pressure. The glomerular filtration rate is thus severely depressed in indomethacin pretreated dogs. Urine and electrolyte excretion is comparably redcued during elevated intrarenal pressure in non-pretreated and in indomethacin pretreated dogs, which suggests that factors other than glomerular filtration rate are involved. Urine osmolarity is positively correlated with renal blood flow, and urine osmolarity increases during elevated intrarenal pressure in non pretreated dogs, whilst urine osmolarity remains unchanged in dogs pretreated with indomethacin.

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1. The antihypertensive agent pinacidil is eliminated from the body mainly by biotransformation in the liver, followed principally by renal excretion of the metabolites. 2. The metabolism and elimination of pinacidil is similar in rat, dog and man, and is independent of the route of administration. 3. After an oral dose, the 24 h urinary excretion of unchanged pinacidil is 13, 4, and 5% in rat, dog and man, respectively. Faecal excretion in the rat and dog is 2 and 4%. 4. In rat, dog and man the main biotransformation product is the pyridine-N-oxide of pinacidil. Following oral administration of pinacidil, 40, 54 and 54%, respectively, is excreted in the urine as the N-oxide during the first 24 h, and less than 1% in the faeces in rat and dog. 5. Three unidentified minor metabolites were found in plasma, urine and faeces in rat and dog. 6. The major metabolite, the pyridine-N-oxide of pinacidil, has an anti-hypertensive potency about a quarter of that of pinacidil. In animals and human volunteers with normal kidney function, however, the plasma concn. of the N-oxide are always lower than those of the parent compound, so that the metabolite contributes little to the antihypertensive effect of pinacidil.

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The liver oils of six different shark species have been analyzed by supercritical fluid chromatography (SFC). The liver oils were from the species Pseudotriakis microdon (False catshark), Centroscymnus coelepsis (Portuguese dogfish), Centrophorus squanosus (Leafscalp gulper shark), Deanea calceus (Birdbeak dogfish), Etmopterus princips (Greater lantern shark), and Centroscymnus crepidater (Longnose velvet dogfish). The method was capable of direct quantitation of squalene and cholesterol, while quantitation of triacylglycerols, cholesterol esters, and diacylglycerol ethers required thin-layer chromatographic fractionation prior to SFC analysis. The iodine values of the liver oil samples gave a linear correlation when plotted against the squalene content found by SFC. The variation of squalene content within one shark species is large, and there are large differences in squalene content from species to species. The squalene contents varied between 0.22 and 82.54 wt%. The identity of the glycerol ethers was investigated by SFC of the unsaponifiable matter. The major glycerol ethers contained chimyl, batyl, and selachyl alcohol. JAOCS 74, 497-503 (1997).