High fat diet increases salt sensitivity and promotes metabolic disorder‐independent hypertension in Dahl salt sensitive rats

Abstract

Salt sensitivity of blood pressure is common in obesity associated hypertension and may have a neurogenic basis. We and others have previously reported that high fat (HF) diet promotes hypertension in Dahl salt sensitive (SS) male rats ingesting a “normal” salt diet (0.33% NaCl). It is unclear if a low salt intake would reduce blood pressure in this model of obesity‐associated hypertension. Therefore in the current study Dahl SS rats were fed a normal fat (NF, 10% kcal from fat) and HF (60% kcal from fat) diet with different salt contents for 24–26 weeks after weaning (3 weeks of age). In rats fed a diet containing 0.24–0.33% NaCl (the normal salt content (NS) in rodent diets), HFNS (n=9) rats had a much higher MAP than NFNS rats (n=10) at the end of the study (158±1 mmHg versus 130±1 mmHg, P<0.05), confirming our previous findings. However, in low salt fed rats (LS, 0.1% NaCl), MAP at the end of the study was only slightly higher in HFLS (n=4) than NFLS (n=5) rats (131±1 mmHg vs 121±3 mmHg, P<0.05). Body weight was not significantly greater, but visceral adipose accumulation was higher, in HFNS and HFLS rats compared to NFNS and NFLS fed rats, respectively. HF fed rats did not show significant alterations in plasma levels of fasting glucose, insulin, leptin, aldosterone and serum creatinine compared to NF rats. Only HFNS rats showed hyperlipidemia and only NFLS rats showed lower plasma urea BUN levels than the other groups of rats. HFNS rats had a larger depressor response to ganglion blockade than did NFNS rats, but this was not observed in HFLS rats compared to NFLS animals. HF diet did not affect the mesenteric arterial (MA) contractile responses to neurotransmitters (norepinephrine and ATP), but MA from HFNS rats exhibited significantly increased wall‐thickness (and cardiac hypertrophy) compared to NFNS rats. Morphological studies did not reveal greater fibrosis in adventitia of mesenteric, intrarenal or coronary arteries in HF rats, suggesting arterial hyperplasia accounted for arterial remodeling in HFNS rats. Our studies suggested that obesity‐associated hypertension in Dahl SS rats is salt‐sensitive and neurogenic, but not associated with obvious metabolic disorders.Support or Funding InformationSupported by NIH2P01HL070687‐11A1