Involvement of prostaglandins and renal haemodynamics in salt-sensitivity of young spontaneously hypertensive rats.
OBJECTIVE
To clarify the involvement of prostaglandins and renal haemodynamics in the pathogenesis of salt-induced hypertension.


METHODS
Young (6-week-old) spontaneously hypertensive rats (SHR), a salt-sensitive hypertensive model, were used.


METHODS
The effect of long-term (4-week) administration of cicletanine (50 mg/100 g in the diet), which stimulates prostaglandins synthesis, was examined concerning the development of hypertension in young SHR fed on 8% salt-containing diet. Whether the cyclo-oxygenase inhibitor indomethacin (3.0 mg/kg per day for the last 4 days of the treatment) attenuates the hypertension was also studied. Renal haemodynamics were examined by clearance of inulin (glomerular filtration rate) and para-aminohippurate (renal plasma flow).


RESULTS
Salt loading significantly accelerated the development of hypertension, and the salt-induced blood pressure rise was significantly attenuated by cicletanine, although cicletanine did not attenuate the spontaneous development of hypertension. The hypotensive effect of cicletanine was abolished by indomethacin. Glomerular filtration rate and renal blood flow were not changed with these treatments. However, the changes in renal vascular resistance were parallel to those in mean blood pressure: it was increased with salt loading, reversed by cicletanine and increased by indomethacin. Salt loading decreased urinary prostaglandin E2, cicletanine reversed the effect of salt loading and indomethacin inhibited the effect of cicletanine.


CONCLUSIONS
The present findings suggest that the abnormality in prostaglandin E2 contributes to the increased salt sensitivity in young SHR, probably through renal haemodynamic changes.
Ando
K
K
Fourth Department of Internal Medicine, University of Tokyo School of Medicine, Japan.
Ono
A
A
Sato
Y
Y
Fujita
T
T
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D015232:Dinoprostone / Q000502:physiology; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011453:Prostaglandins / Q000502:physiology*; D011725:Pyridines / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D012079:Renal Circulation / Q000187:drug effects / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
D011453:Prostaglandins; D011725:Pyridines; D012965:Sodium Chloride; C038068:cicletanine; D015232:Dinoprostone; D007213:Indomethacin