THE EFFECTS OF HIGH SALT DIET AND EXERCISE ON THE WATER-SALT BALANCE AND BLOOD PRESSURE IN RATS
Abstract views: 157
/ 
PDF downloads: 204
DOI:
https://doi.org/10.26900/jsp.5.1.05Keywords:
Hypertension, Intensive Exercise, Intrarenal Dopamine, Oxidative StressAbstract
In the study which was prepared based on the factors that can take place in essential hypertension pathology; We aimed to investigate the interactions of intensive exercise, high salt and partial NOS inhibition applications with each other, the effects on water-salt balance and blood pressure, changes in the intrarenal dopaminergic system, which is an important natriuretic system, and the participation of oxidative stress. The rats were given intensive exercise on a treadmill at a speed of 25 m / min at 5% inclination for 30 minutes a day, LNNA at a concentration of 50 mg / L and a high salt diet of 4% for 7 days either separately or together. Blood pressures of the rats were measured on the first and last days of the experiment, and the rats were taken into metabolic cages; 24-hour water intake and urinevolume were measured. Dopamine levels were measured in 24-hour urine to detect intrarenal dopamine synthesis. In addition, oxidative stress parameters in the serums of rats; TAS, TOS and OSI levels were measured. Blood pressure was found to be high in the groups in which intensive exercise was applied together with LNNA and high salt diet. While there was no change in the water balance of this group, it was found that sodium excretion and dopamine levels increased in 24-hour urine. In addition, it was found that the total oxidant status increased in this group, and oxidative stress developed as a result of insufficient antioxidant system. It suggests that the reason of hypertension that develops with the application of intensive exercise together with LNNA and high salt diet may be due to the vascular resistance increasing effect of oxidative stress rather than water-salt retention and it points out the necessity of studies to fully detect vascular tissue oxidative stress markers and vascular oxidative damage.
Downloads
References
AEKTHAMMARAT, D., PANNANGPETCH, P., et al. (2019). Moringa oleifera leaf extract lowers high blood pressure by alleviating vascular dysfunction and decreasing oxidative stress in L-NAME hypertensive rats. Phytomedicine, 54, 9-16.
ALESSIO, H.M. (1993). Exercise-Induced Oxidative Stress. Medicine and Science in Sports and Exercise, 25, 218-224.
ARAKAWA, K., MIURA, S., et al. (1995). Activation of renal dopamine system by physicalexercise. Hypertens Res., 18, 573-577.
BANDAY, A.A. and LOKHANDWALA, M. (2020a). Renal dopamine oxidation and ınflammation in high salt fed rats. Journal of the American Heart Association, 9(1), e014977.
BANDAY, A.A., LAU, Y.S., et al. (2008b). Oxidative stress causes renal dopamine d1 receptor dysfunction and salt-sensitive hypertension in sprague-dawley rats. Hypertension, 51, 367-375.
BAYLİS, C., HARTON, P., et al. (1990). Endothelial derived relaxing factor controls renal hemodynamics in the normal rat kidney. J Am Soc Nephrol, 1(6), 875-81.
BERGHOLMA, R., MÄKIMATTILAA, S., et al. (1999). Intense physical training decreases circulating antioxidants and endothelium-dependent vasodilatation in vivo. Atherosclerosis, 2, 341–349.
CAREY, R.M. (2001). Renal dopamine system: paracrine regulator of sodium homeostasis and blood pressure. Hypertension, 38, 297-302.
CHAMPLAIN, J., WU, R., et al. (2004). Oxidative stress in hypertension clinical and experimental hypertension. J Hypertens, 7-8, 593-601.
CHRYSANT, S.G. (2016). Effects of high salt intake on blood pressure and cardiovascular disease: The role of COX inhibitors. Clinical Cardiology, 39(4), 240-242.
CORNELİSSEN, V.A. & SMART, N.A. (2013). Exercise training for blood pressure: a systematic review and meta‐analysis. Journal of the American heart association, 2(1), e004473.
EREL, O. (2005a). New automated colorimetric method for measuring total oxidant status. Clinical Biochemistry, 12, 1103–1111
EREL, O. (2004b). Novel automated direct measurement method for total antioxidant capacity using a new generation, more stable ABTS radical cation. Clinical Biochemistry, 4, 277–285.
FENG, W., DELL’ITALIA, L.J., et al. (2017). Novel paradigms of salt and hypertension. Journal of the American Society of Nephrology, 28.5, 1362-1369.
GRANGER, J.P. & ALEXANDER, B.T. (2000). Abnormal pressure-natriuresis in hypertension: role of nitric oxide Acta Physiol , Scand., 168, 161-168.
HEGDE, S.M. & SOLOMON, S.D. (2015). Influence of physical activity on hypertension and cardiac structure and function, Current hypertension reports, 17.10: 77.
HUSAIN, K. (2003). Interaction of exercise training and chronic NOS inhibition on blood pressure, heart rate, NO and antioksidants in plasma of rats. Pathophysiology, 10, 47-53.
JI, L.L, GOMEZ, M.C, et al. (2004a). Acute exercise activates nuclear factor (NF)-signaling pathway in rat skeletal muscle. FASEB J., 18, 1499–1506.
JIL, L.L. (1999). Antioxidants and oxidative stress in exercise. exp Biol Med., 3, 283-292.
JOHNSON, R.A. & FREEMAN, R.H. (1992). Pressure natriuresis in rats during blockade of the L-arginine/nitric oxide pathway Hypertension. Acta Clinica Belgica, 19, 333-338.
KITIYAKARA, C., CHABRASHVILI, T., et al. (2003). Salt intake, oxidative stress and renal expression of NADPH oxidase and superoxide dismutase. J Am Soc Nephrol, 14(11), 2775-82.
KOPKAN, L. & MAJID, D.S. (2005). Superoxide contributes to development of salt sensitivity and hypertension induced by nitric oxide deficiency. Hypertension, 46, 1026-31.
KURU, O, SENTURK, U.K., et al., (2009). Effect of exercise training on resistance arteries in rats with chronic NOS inhibition. J Appl Physiol, 107, 896–902.
LENDA, D.M., SAULS B., et al., (2000). Reactive oxygen species may contribute to reduced endothelium-dependent dilation in rats fed high salt. American Journal of Physiology - Heart and Circulatory P. hysiology, 279, 7-14.
LOPERENA, R. & HARRISON D.G. (2017). Oxidative stress and hypertensive diseases. Medical Clinics.,101(1), 169-193.
MAEDA, H., SASAGURI, M., et al. (2000). Roles of renal dopamine and kallikrein-kinin systems in antihypertensive mechanisms of exercise in rats. Hypertens Res., 23, 511-519.
MAJID, D.S. & KOPKAN, L. (2007). Nitric oxide and superoxide interactions in the kidney and their implication in the development of salt-sensitive hypertension. Clin Exp. Pharmacol Physiol, 34, 946-52.
MANNING, R.D., HU, L., et al. (1993). Cardiovascular responses to long-term blockade of nitric oxide synthesis. Hypertension, 22, 40-8.
MARK, A.L., LAWTON, W.J., et al. (1975). Effects of high and low sodium intake on arterial pressure and forearm vasular resistance in borderline hypertension. Circulation Research, 36, 194-198.
MENTE, A., O'DONNELL, M. J., et al. (2014). Association of urinary sodium and potassium excretion with blood pressure. New England Journal of Medicine, 371(7), 601-611.
NAPOLI, C. & IGNARRO L.J. (2009). Nitric oxide and pathogenic mechanisms involved in the development of vascular diseases. Arch Pharm Res., 32, 1103-1108.
POWERS, S.K, & JACKSON, M.J. (2008). Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production. Physiol Rev., 88(4), 1243–1276.
SCHULTZ, M.G, GERCHE, L., et al. (2017). Blood pressure response to exercise and cardiovascular disease. Current hypertension reports, 19.11, 89.
SHULTZ, P.J. & TOLINS, P.J. (1993). Adaptation to increased dietary salt intake in the rat role of endogenous nitric oxide. J. Clin. Invest., 91, 642-65.
TABET, F., SAVOIA, C., et al. (2004). Differential calcium regulation by hydrogen peroxide and superoxide in vascular smooth muscle cells from SHR, J Cardiovasc Pharmacol.,44, 1–9.
TITZE, J., & LUFT, C.F. (2017). Speculations on salt and the genesis of arterial hypertension. Kidney International, 91, 1324–1335.
TOLINS, J.P. & SHULTZ, P.J. (1994). Endogenous nitric oxide synthesis determines sensitivity to the pressor effect of salt, Kidney Int. 46, 230-6.
TOUYZ, M.R. (2004). Reactive oxygen species, vascular oxidative stress, and redox signaling in hypertension: what ıs the clinical significance? Hypertension, 44, 248-252.
VAPAATALO, H., MERVAALA, E., et al. (2000). Role of endothelium and nitric oxide in experimental hypertension. Physiol Res., 49,1-10.
VAZIRI, N.D., WANG, X.Q., et al. (2000). Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. Hypertension, 36, 142-6.
WANG, Z.Q., SIRAGY, H.M, et al., (1997). Intrarenal dopamine production and distribution in the rat: physiological control of sodium excretion. Hypertension, 29, 228–234.
WAYNE, A.R., GILL, J.R., et al. (1974). Effects of dietary sodium and of acute saline ınfusion o the ınterrelationship between dopamine excretion and adrenergic actity in man, The Journal of Clinical Investigation, 54, 194-200.
WILCOX, S.C. (2005). Oxidative stress and nitric oxide deficiency in the kidney: a critical link to hypertension? American Journal of Physiology Regulatory. Integrative and Comparative Physiology, 289, 583–597.
WITT, E.H. & REZNICK, A.Z., et al. (1992). Exercise, Oxidative Damage and the Effects of Antioxidant Manipulation, J. Nutr., 122, 766-73.
XU, J., LI, X.X., et al. (2000). D1 receptor, gsα, and na+/h+ exchanger ınteractions in the kidney in hypertension. Hypertension. 36, 395–399.
YUASA, S., LI, X., et al. (2000). Sodium sensitivity and sympathetic nervous system in hypertension ınduced by long-term nitric oxide blockade in rats. Clin Exp Pharmacol Physiol, 27, 18-24.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2021 Holistence Publications
This work is licensed under a Creative Commons Attribution 4.0 International License.
When the article is accepted for publication in the HSQ authors transfer all copyright in the article to the Holistence Academy Ar-Ge Yazılım Yayıncılık Eğitim Danışmanlık ve Organizasyon Ticaret Ltd. Şti.The authors reserve all proprietary right other than copyright, such as patent rights.
Everyone who is listed as an author in this article should have made a substantial, direct, intellectual contribution to the work and should take public responsibility for it.
This paper contains works that have not previously published or not under consideration for publication in other journals.
