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To discuss the relationship of salt sensitivity and the renin-angiotensin system.

Article inclusion criteria not specified.

Not specified.

Recruitment: Article selection methods not specified.  56 articles referenced.

Design: Narrative review.

Blinding (if applicable): not applicable

Intervention (if applicable): not applicable

Statistical Analysis: not applicable

Timing of Measurements: not specified

Dependent Variables:

• Renin-angiotensin system

Independent Variables:

• dietary salt intake

Control Variables:

Initial N: Not included

Attrition (Final N): Not included

Age: Not included

Ethnicity: Not included

Other Relevant Demographics: Not included

Anthropometrics: Not included

Location: Not included

Salt and cardiovascular structure and function

1. Essential hypertensives with microalbuminuria also have increased cardiovascular morbidity and mortality because of the striking cluster of metabolic risk factors associated with their increased blood pressure, such as insulin resistance, blood pressure salt sensitivity, dyslipidemia, endothelial dysfunction and loss of normal diurnal variation of blood pressure.

2. Several clinical studies have demonstrated that the greater the dietary salt consumption, the greater the likelihood of left ventricular hypertrophy. Strong epidemiological evidence supports the concept that increases in left ventricular mass are important risk factors for cardiovascular morbidity and mortality.

3. Increasing dietary salt intake and retention appears to affect vascular compliance independent of blood pressure, specifically in individuals who have pressor responses to dietary salt consumption and in the elderly.

4. There is a striking correlation between median 24-hr urinary sodium excretion levels and stroke mortality in the WHO mortality rates from the Intersalt Study.

Salt sensitivity of blood pressure: a renal hemodynamic abnormality

1. There is diminished effective renal plasma flow in response to greater dietary salt intake in salt sensitive individuals with hypertension. However, the exact mechanism for this is unknown.

Salt, hypertension and glomerular injury in diabetes

1. In diabetics, there is evidence of inadequate renal autoregulation of blood flow, in that for any given pressure, there is greater transmission of systemic pressure to the glomerulus. This results in greater glomerular capillary pressure, proteinuria, and progressive renal injury.

2. Results from clinical trials demonstrate that a systolic blood pressure of <130 mm Hg is recommended to lessen the risk of renal injury.

a. In the Diabetic Nephropathy Study, a systolic blood pressure of 126 mm Hg correlated with preservation of renal function compared to a systolic pressure of 140 mm Hg.

Pharmacologic blockade of the renninangiotensin system: An appropriate therapeutic target

1. The renin-angiotensin system has been implicated in the development of hypertension, microalbuminuria and target organ damage in diabetics.

2. Clinical studies have demonstrated that greater dietary salt consumption in essential hypertensives resulted in variable suppression of the renin-angiotensin system and that a more pronounced decrease in plasma renin activity coincided with greater renal vasodilation as measured by enhanced renal blood flow.

3. Clinical studies utilizing either renin inhibitors or ACE inhibitors have demonstrated that these therapies can lead to an increase in renal blood flow despite greater dietary salt consumption in patients with suppressed plasma renin activity.

4. The research data strongly suggest that greater dietary salt consumption should not result in an increase in blood pressure if there is an adequate rise in renal blood flow and GFR through the suppression of the intrarenal rennin-angiotensin system.

Not only is dietary salt restriction important from a hemodynamic and structural standpoint, it can also affect the antiproteinuric properties of both ACE inhibitors and nondihydropyridine calcium channel blockers. Is it possible that inadequate reduction of dietary salt defines a population of patients who do not demonstrate benefit from ACE inhibition in delaying progression of renal disease?

It is clear that efforts should be made to reduce dietary salt consumption as best as possible in diabetic hypertensive patients, not only to reduce the likelihood of salt-induced target organ damage, but also to potentiate the antihypertensive and antiproteinuric activities of drugs that block the renin-angiotensin system.

University/Hospital:

University of Maryland School of Medicine,

This review gives a strong argument for encouraging individuals with diabetes and hypertension to follow a diet low in sodium (~2 g/d) to potentiate the effects of ACE inhibitors and calcium channel blockers in the treatment of hypertension.