Renin and Hypertension Low renin and High Renin essential hypertension

  • Renin is enzyme secreted by juxtaglomerular cells of the kidney.
  • Hypertensives can be low renin essential
  • Hypertensives and high renin essential hypertensives.

Low renin essential hypertension :

  • 20% of pa­tients of essential hypertension have low renin es­sential hypertension.
  • When patients with low renin essential hypertension take sodium-rich diet,
  • their aldosterone suppression does not occur, lead­ing to hyperaldosteronism causing more sodium re­tention, volume expansion and high BP.
  • There is increased ‘mineralocor­ticoid production, leading to increased sodium reten­tion, which in turn causes renin suppression.
  • The ad­renal cortex of low renin hypertensives have increased sensitivity to angiotensin II.
Renin and Hypertension 1

hypertension and renin

Non modulating essential hypertension :

  • The adrenal or renal vascular responses to angiotensin II is not modulated by sodium intake.
  • The effect of an­giotensin II does not depend on sodium intake in these patients.
  • so salt intake should be low. –
  • There is insulin resistance.
  • Non-modulation is a genetic problem.
  • 30% of hypertensives are non-modulating essential hypertensives.
  • Plasma renin activity levels are normal to high.
  • – Kidneys are unable to excrete sodium appropriately


  • ACE inhibitors and salt restriction.
  • High Renin Essential Hypertension (HREH)  15% of hypertensives have HREH.
  • There is increased adrenergic system activity.
  • Angiotensin receptor blockers may or may not be effective.

Salt intake:

  • Higher the salt intake more the BP es­pecially in primary aldosteronism, bilateral renal ar­tery stenosis, renal parenchymal disease, low renin essential hypertension.
  • Salt includes chiefly – Sodium Chloride Calcium

Sodium, Chloride and Calcium

  • NaCI increases blood pressure.
  • Na without chloride does not increase blood pres­sure.
  • Intracellular calcium can lead to hypertension .
  • Calcium _entry blokers are very potent Fntihypertensives.
  • Low calcium intake also results in hypertension.

Cell membrane defect:

  • Abnormalities of sodium transport occur.
  • There is abnormal accumulation of calcium in vascular smooth muscle leading to vaso­constriction and hypertension.
  • This defect is present in of hypertensives.

Insulin resistance :

  • is related to hypertension. In­sulin resistance is common in obesity and NIDDM.
  • Obesity and NIDDM are common in hypertensives. These together form the metabolic syndrome also called syndrome X.

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