Patients with elevated blood pressure should follow a weight-reducing diet, take regular exercise, and restrict alcohol and salt intake. Available evidence does not support relaxation therapies, calcium, magnesium or potassium supplements to reduce blood pressure.
Daily sodium excretion by kidneys is depends on blood hydro static pressure on kidneys arterioles. The more blood pressure, the more daily sodium excretion. In order to balance total daily sodium input and out put, kidneys regulate blood pressure at a point that it would maintain sodium balance. Therefore more sodium intake needs more blood pressure in order to kidneys can excrete same amount of sodium. Relationship between pressure and sodium excretion by kidneys is demonstrated as pressure-natriuresis curve.This curve vary in different people and depends on genetic and acquired variables.
Moderate to intensive physical exercise may decrease your blood pressure by 10 mm Hg. You might then apply the Wilder's principle (see Franz Messerli Eur Heart J in press) and understand that the higher your baseline blood pressure, the more important this effect.
Moderate salt reduction up to a NaCl secretion of 5 gr/24 hours is beneficial, decreases BP by 5-8 mmHg and sensitises your vessels to the effect of RAS inhibitors, similarly as diuretics but to a lesser extent. More severe reduction of salt intake however has shown to be associated with poorer outcome (Salim Yusuf, PMID: 23257945).
The basic defect in primary hypertension is the inability of the kidneys to excrete the excess salt to maintain homeostasis . Therefore , those who consume less salt will not develop hypertension , while those who consume high salt , some will develop hypertension , due to renal excretion defect , which is probably genetic in origin . The excess retained salt would initially produce increased cardiac output causing hypertension , but later , due to local auto - regulation of various organs , there is increased peripheral resistance , which becomes the main cause of hypertension ( Guyton's hypothesis ) . This occurs as a trade off due to natriuretic hormones , which cause natriuresis & salt excretion , but with increased peripheral vascular resistance due to retention of sodium in the vascular cells due to dysfunction of the Na - K ATPase pump , which maintains the hypertension . This hypothesis links the role of salt in causing hypertension . In addition , the sympathetic system & the Renin - Angiotensin system play an important role .
Therefore , the intake of low salt would prevent hypertension in normal individuals , but in the treatment of hypertension it would cause only a small decline of BP . Diuretics & salt restriction alone would not control hypertension & would need to be combined with other drugs . The policy to decrease salt intake would definitely be a valuable preventive public health tool to prevent the development of hypertension in normal population .
If you are looking for a way to quantify a patient's response to salt reduction or exercise, you could consider using impedance cardiography (ICG). For salt reduction, favorable changes would be expected in the ICG measurements of cardiac index (cardiac output divided by body surface area), systemic vascular resistance, and the level of thoracic fluid. In response to exercise, favorable changes would be expected in left ventricular contractility, systemic vascular resistance, pulse pressure, and arterial compliance. The ICG parameters are described in the attached paper.
Article Using impedance cardiography with postural change to stratif...
J. Yaberi's answer entails statements that are, at best, misleading (e.g., "Daily sodium excretion by kidneys is depends on blood hydro static pressure on kidneys arterioles."). Of course, hydrostatic pressure in the glomarular capillaries is needed as the driving force for filtration, yet - as long as GFR is not compromised - the amount of Na and water that is excreted per time is determined by tubular resorption which is governed by multiple humoral (e.g., RAAS, Vasopressin) and nerval factors. Also, his response relays grossly oversimplified ideas (e.g., "Therefore more sodium intake needs more blood pressure in order to kidneys can excrete same amount of sodium.") taken from the concept of the "renal body fluid pressure control system" first proposed by Borst & Borst-DeGeus 1963 and later on elaborated and promoted by Guyton (also mentioned in the answer by Singh Shivakumar). Guyton, however, was fully aware at his time already, that arterial pressure does not increase with Na intake as long as the RAAS is fully operative (see y-axis parallel pressure in so-called chronic renal function curves of healthy subjects). In addition, it should be noted that Guyton's concept has been pruned and re-shaped in several regards within the last 15 years according to new results obtained by various labs.
Just stumble into this question - probably not relevant but would like to add that not all ionic salts increase BP. Potassium/sodium nitrate (via entero-salivary circulation of nitrate) for example, potently reduce resting BP (e.g −9.4 mmHg using 12 mmol KNO3). On top of that, 7 to 25% (dose dependent) exercise tolerance improvement was also reported using dietary nitrate.
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