Function of the arachidonate-deficient spontaneously hypertensive rat kidney.
In order to assess the effect of renal prostaglandins on the glomerular filtration rate (GFR) and electrolyte excretion in the spontaneously hypertensive rat (SHR), we perfused isolated SHR and normotensive Wistar-Kyoto (WKY) kidneys after pretreatment with either a control diet or a diet deficient in arachidonate, the precursor of prostaglandins. When perfusion pressures were increased from 100 to 160 mm Hg, renal vascular resistances (RVR) increased by 32-41%. RVR of SHR kidneys always exceeded that of WKY kidneys by a nearly constant amount, and arachidonate deficiency had little effect on this relationship. In contrast to RVR, the GFR increased severalfold. GFR and urine flow were greater in WKY than in SHR kidneys, a relationship unaffected by arachidonate deficiency. Changes in sodium and chloride excretion occurred in parallel with GFR. Although arachidonate-deficient SHR and WKY kidneys manifested potassium wastage compared to controls, arachidonate deficiency did not result in altered sodium or chloride excretion. The results suggest that direct actions of arachidonate or renal prostaglandins are not responsible for most functional differences between SHR and WKY kidneys.
D000818:Animals; D001095:Arachidonic Acids / Q000172:deficiency*; D002712:Chlorides / Q000378:metabolism; D005919:Glomerular Filtration Rate; D006977:Hypertension, Renal / Q000503:physiopathology / Q000662:veterinary*; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012376:Rodent Diseases / Q000503:physiopathology*; D012964:Sodium / Q000378:metabolism; D014655:Vascular Resistance
D001095:Arachidonic Acids; D002712:Chlorides; D011453:Prostaglandins; D012964:Sodium