ABSTRACT
Salt-induced hypertension presents a significant health threat with deleterious cardiovascular events and cellular damage, whereas heat shock protein 70 (HSP70) is a molecular chaperone that mitigates pathologic stress-induced cellular processes. This study aimed to examine the influence of heat shock protein 70 (HSP70) on the Sprague-Dawley rats model of salt-induced hypertension and modulation by antioxidants and antihypertensive drugs. Thirty-six male Sprague-Dawley rats were assigned to different groups receiving a high-salt diet with various interventions. The control group received a standard rat chow diet (0.3% NaCl) and water. Others were fed on high salt diet (8% NaCl) with interventions including Lisinopril, Losartan, Verapamil, Vitamin C, Magnesium, Kolaviron, and a combination of antioxidants. After 8 weeks of experimentation, within which blood pressure and heart rate were monitored using the tail-cuff method, animals were sacrificed, and blood samples were collected for cortisol, nitric oxide, and endothelin-1 analyses. The left ventricle was harvested for HSP70 gene expression using the Western blot procedure. Results reconfirmed a high salt diet significantly increased systolic, diastolic, and mean arterial pressure and heart rate. The Lisinopril, Losartan, Verapamil, Vitamin C, and Magnesium groups demonstrated significant blood pressure reduction. Furthermore, HSP70 expression was significantly reduced in the high salt group compared to the control. Losartan, Verapamil, Vitamin C, Magnesium, Kolaviron, and Vit+Mg+Kv significantly increased HSP70 levels under high salt conditions, suggesting their modulation effects. Further insights emerged from a significant positive correlation between HSP70 levels and the mean arterial pressure in the high salt plus anti-hypertensive groups and a negative correlation in the antioxidant groups, unveiling an intricate modulation interplay between HSP70, antioxidants and antihypertensives in animal models of salt-induced hypertension. This contributes valuable insights into potential therapeutic strategies for managing salt-sensitive hypertension. The observations underscore the need for further exploration in clinical settings to enhance a proper understanding of this complex relationship.
