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.

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

Treatment –

• 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.