{'fraction_non_alphanumeric': 0.010091743119266056, 'fraction_numerical': 0.0009174311926605505, 'mean_word_length': 5.734567901234568, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Nifedipine--studies on its mechanism of action and interaction with other circulatory control mechanisms in man.

Calcium antagonists such as nifedipine have been shown to lower blood pressure alone or in combination with other drugs in mild, moderate and severe hypertension. It is likely that the antihypertensive action depends on modification of calcium dependent coupling of excitation and contraction in peripheral vascular smooth muscle. Acute effects of nifedipine are associated with reflex mediated increases in sympathetic tone and plasma renin activity while in the long term these effects are less prominent. Nifedipine does not interfere with depressor mechanisms mediated by prostaglandins or peripheral vascular beta 2 receptors. In contrast peripheral pressor mechanisms including those mediated by angiotensin II and noradrenaline are antagonised. The long term efficacy of nifedipine in hypertension probably depends on its direct vasodilator effect, the preservation of depressor mechanisms and attenuation of reflex responses and direct and indirect pressor mechanisms.