Abstract
Amongst specific causes of secondary hypertension renovascular hypertension remains the second most common form which frequently presents with resistance to pharmacologic treatment. Activation of both the renin–angiotensin system and the sympathetic nervous system are well recognized mechanisms involved in renovascular hypertension as evidenced by increased plasma renin activity and angiotensin II levels, as well as increased rates of efferent sympathetic-nerve firing and total body noradrenaline spillover [1,2].
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