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THE INFLUENCE OF RENAL PROSTAGLANDINS, CENTRAL NERVOUS SYSTEM AND NaCl ON HYPERTENSION OF DAHL S RATS
Author(s) -
Tobian Louis,
Ganguli Mukul,
Goto Atsuo,
Ikeda Toshio,
Johnson Mary Ann,
Iwai Junichi
Publication year - 1982
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1982.tb00818.x
Subject(s) - medicine , endocrinology , linoleic acid , arachidonic acid , renal papilla , chemistry , prostaglandin , prostaglandin e2 , kidney , biology , fatty acid , biochemistry , enzyme
SUMMARY 1.Kidney factors and central nervous system (CNS) factors appear to have powerful influences on NaCl‐induced hypertension. In quick‐frozen kidneys the prostaglandin E 2 (PGE 2 ) concentration in the renal papilla is 60% lower in Dahl S rats than in Dahl R rats (17 ng/100 mg vs 42 ng/100 mg; P <0.01) when both S and R rats are on a 0.3% low NaCl diet. When S and R rats eat a 4% high NaCl diet for 4 weeks or 11 weeks, the PGE 2 concentration doubles in both strains ( P <0.05) but the papillary PGE 2 concentration in the S rats is always about half that in the R rats ( P <0.01). 2.Through effects on Na excretion and papillary plasma flow, the low PGE 2 in S papillas may account in part for the large rises of blood pressure in S rats after eating a high NaCl diet. This proposition was explored by utilizing high fat diets with either normal or high linoleic acid content. Arachidonic acid is the precursor of PGE 2 and linoleic acid is the precursor of arachidonic acid. It turned out that the low PGE 2 level in S papillae could be tripled by a diet high in linoleic acid. Sixteen S rats on a 16 week diet with 5% NaCl/1.5% linoleic had a mean papillary PGE 2 level of 30 compared to a level of 89 in fifteen other S rats on a diet with 5% NaCl/16% linoleic. The 16% high linoleic diet tripled the PGE 2 concentration in S papillae ( P < 0.005). It also increased the PGE 2 concentration in R papillae 2.5 times, 137 vs 53 ( P <0.02). On either high or normal linoleic diets the PGE 2 in S papillae was always at least 35% less than that in R papillae. However the 16% high linoleic diet did raise the papillary PGE 2 level in S rats up to that found in normal rats on regular rat chow of equivalent NaCl content. Moreover this change in PGE 2 level was associated with greatly reduced blood pressure rises in S rats. 3. The blood pressures of S rats on a 5% NaCl/1.5% linoleic diet began to rise after 5 weeks on the diet and reached 183 mmHg after 16 weeks. The blood pressures of S rats on a 5% NaCl/16% linoleic diet did not begin to rise until 12 weeks on the diet and reached only 166 after 16 weeks. The high linoleic diet greatly delayed the onset of the rise in blood pressure and significantly reduced the ultimately attained level ( P < 0.001). In fact, on a low 0.3% NaCl diet, S rats of comparable age will reach approximately the same mildly hypertensive level of 166. Thus in S rats the high linoleic diet brings papillary POE 2 up to normal and also prevents the large rises in blood pressure usually related to a high NaCl intake. These two changes may well be causally related. 4. The CNS also influences NaCl hypertension in S rats. Bilateral electrolytic lesions of the paraventricular nuclei bordering the third brain ventricle cause S rats to attain only half of the NaCl‐induced hypertension seen in sham‐lesioned S rats (163 vs 197 mmHg, P < 0.001). Destroying catecholaminergic neurons in the brain of S rats using 6‐hydroxydopamine put into the lateral brain ventricle also abolishes half of the NaCl hypertension (165 vs 210; P <0.001). Bilateral lesions of the suprachiasmatic nuclei near the third brain ventricle significantly worsen NaCl hypertension in S rats (blood pressure 201 with SCN lesions vs blood pressure 186 with sham lesions, P <0.001). Thus the kidney, the CNS and sodium influence the degree of hypertension in the Dahl S rat.