Treating High Blood Pressure (Hypertension) with Physical Activity and Reduced Salt Intake | Mukaila Kareem, DPT | RxEconsult
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Effect of Salt Intake and Physical Activity on Hypertension (High Blood Pressure) Category: Hypertension by - April 19, 2014 | Views: 51533 | Likes: 3 | Comment: 3  

High Blood Pressure or Hypertension

Hypertension or high blood pressure is defined as having a systolic blood pressure at and above 140 mmHg or a diastolic blood pressure of 90 mmHg and above. The term essential hypertension is often used because about 90% of hypertension is unknown but combined factors of genetic, environment, physical inactivity, aging and smoking are implicated. It is a major risk factor for heart disease and stroke with a prevalence of about 67millions among Americans. Hypertension accounts for one out of every seven deaths and about 70% of patients with first heart attack, stroke or history of heart failure are hypertensive. A normotensive individual at the age of 55 years has 90% estimated risk of developing hypertension for the remainder of his/her lifetime.

 

Also Read: What is your Blood Pressure 

 

Several decades of research point to a strong relationship between excessive ingestion of salt and hypertension. Humans naturally handle a total of 2.5 grams of salt per day but the amount of salt per day in a typical US diet is about 9.6 grams. The sources of salt ingestion in modern society are processed foods (75%), cooking plus table salt (15%), and only 10% is attributable to natural sources. Hence, 90% of salt intake in western population is manufactured!

The kidney is the main source of salt excretion and therefore maintains normal balance between sodium ingestion, body fluid and long term blood pressure control. It principally functions under the baseline influence of the involuntary nervous system called sympathetic nervous system (SNS). Excessive intake of salt causes increase in sodium concentration in the fluid found in blood and brain called plasma and cerebrospinal fluid respectively. This high sodium concentration triggers over-excitation of the cardiovascular center in the brain and on the SNS that supplies the kidney and other organs. Therefore, for the salt sensitive individuals, hypertension may develop when the kidney is in overdrive trying to get rid of excessive sodium by raising a new blood pressure threshold to maintain stability.

 

Also Read: Renin Angiotensin Aldosterone System and Blood Pressure Control

 

Furthermore, sedentary lifestyle is also a contributor to high blood pressure and has been linked to hyperactivity of SNS. Specifically, physical inactivity facilitates increase in resting renal sympathetic activity. In fact, 40% to 65%  of patients with high blood pressure have 100% to 200%  increase in SNS activity in the brain, heart, kidneys and the blood vessels supplying the skeletal muscles. This induces excessive discharge and low re-uptake of norepinephrine, a neurotransmitter that causes strong contraction of heart muscle and constriction of arterial vessels. Sedentary lifestyle is associated with increase angiotensin II receptors on arterial vessels. Angiotensin II is a potent bioactive substance that binds with angiotensin receptors to induce arterial constriction and contributes to high blood pressure. It is a final product of rennin aldosterone angiotensin system (RAAS) that may result in further retention of sodium and water with continuing hyperstimulation of kidney by the SNS.

As noted, essential hypertension is caused by several factors but it is a modifiable condition that can be controlled or prevented. For instance, through neural adaptation, chronic bouts of exercise have been shown to dampen SNS overstimulation, reduce plasma norepinephrine with decrease vascular tone and consequently lower blood pressure. Additionally, the mechanical effect of physical activity produces shear stress on arterial wall to maintain integrity of blood vessels. This helps to prevent vascular stiffness, decrease angiotensin II receptors, facilitate structural enlargement of blood vessels and induce mechanism that produces endogenous nitric oxide. Nitric oxide is an intermediate molecule that causes vasodilation or expansion of blood vessels and therefore reduces vascular resistance to blood flow. It also prevents overactivity of SNS both in the brain and the peripheral distribution. Regular exercise has the added benefit of improving sensitivity of skeletal muscle and therefore reduces excessive production of insulin, which is also known to be a strong SNS stimulant.

Regular bouts of leisure-time physical activity are known to reduce risk of hypertension, regardless of presence of contributory factors. In fact, exercise acutely reduces blood pressure 4 to 10 hours after exercise and may last up to 22 hours. The general exercise prescription for adults is at least 150 mins per week of aerobic exercise such as brisk walking and 2 days or more of resistive exercise that targets legs, arms, and back. The session can be 30 minutes per day, 15 mins twice daily or 10 mins thrice daily. Other than brisk walking, it is recommended that people who are not physically active should refrain from intense physical activity and hypertensive patients should discuss individualized exercise program with their providers. Studies show that the risk of developing hypertension in physically inactive normotensive men and women is about 35% to 70% higher when compared with physically active peers.  

Physical activity along with pharmacological intervention can help reduce polypharmacy and strict compliance with regular physical activity may prevent onset of hypertension in non-hypertensive individuals. In other words, not all of us are hypertensive but all of us can benefit from positive lifestyle changes with potential to prevent hypertension and by extension reduce the risk of blood pressure associated complications in the society. Readers are encouraged to visit Let's Move, Healthy People 2020 and Centers for Disease Control for other lifestyle modification for management of hypertension in particular and chronic diseases in general.

References

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Bolivar, J. J. (2013). Essential hypertension: An approach to its etiology and neurogenic pathophysiology. International Journal of Hypertension, 2013. Retrieved from www.hindawi.com

Booth, F.W., Chakravarthy, M. V., Gordon, S. E., & Spangeberg, E. E. (2002). Waging war on physical inactivity: Using modern molecular ammunition against an ancient enemy. Journal of Applied Physiology, 93(1). Retrieved from jap.physiology.org

Cordain, L., Eaton, S. B., Sebastian, A., Mann, N., Linderberg, S., Watkins, B. A., O’Keefe, J. H., & Brand-Miller, J. (2005). Origins and evolution of the Western diet: Health implications for the 21st century. The American Journal of Clinical Nutrition, 81(2). Retrieved from ajcn.nutrition.org

Emanus, A., Wilsgaard, T., Furberg, A-S., & Thune, I. (2011). Blood pressure, cardiorespiratory fitness, and body mass: Results from the Tromso Activity Study. Norsk Epidemiologi, 20(2). Retrieved from www.ntnu.no

Kingwell, B. A. (2000). Nitric oxide-mediated metabolic regulation during exercise: Effects of training in health and cardiovascular disease. The Journal of Federation of American Societies for Experimental Biology, 14(12). Retrieved from www.fasebj.org

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Leosco, D., Parisi, V., Femminella, G. D., Formisano, R., Petraglia, L., Allocca, E., & Bonaduce, D. (2013). Effects of exercise training on cardiovascular adrenergic system. Frontiers in Physiology, 4. Retrieved from www.ncbi.nlm.nih.gov

Pedersen, B. K. & Saltin, B. (2006). Evidence for prescribing exercise as therapy in chronic disease. Scandinavian Journal of Medicine & Science in Sports, 16. 

Schlaich, M. P., Lambert, E., Kaye, D. M., Krozowski, Z., Campbell, D. J., Lambert, G., Hastings, J., Aggarwal, A., & Esler, M. D. (2004). Sympathetic augmentation in hypertension: Role of nerve firing, norepinephrine, reuptake, and angiotensin neuromodulation. Hypertension, 43. 

Stocker, S. D., Monahan, K. D., & Browning, K. N. (2013). Neurogenic and sympathoexcitatory actions of NaCl in hypertension. Current Hypertension Reports, 15. 


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