{'fraction_non_alphanumeric': 0.02532617037605526, 'fraction_numerical': 0.0, 'mean_word_length': 6.010752688172043, '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}}
Administration of prostacyclin modulates cutaneous blood flow but not sweating in young and older males: roles for nitric oxide and calcium‐activated potassium channels

In young adults, cyclooxygenase (COX) contributes to the heat loss responses of cutaneous vasodilatation and sweating, and this may be mediated by prostacyclin‐induced activation of nitric oxide synthase (NOS) and calcium‐activated potassium (KCa) channels. This prostacyclin‐induced response may be diminished in older relative to young adults because ageing is known to attenuate COX‐dependent heat loss responses. We observed that, although prostacyclin does not mediate sweating in young and older males, it does modulate cutaneous vasodilatation, although the magnitude of increase is similar between groups. We also found that, although NOS and KCa channels contribute to prostacyclin‐induced cutaneous vasodilatation in young males, these contributions are diminished in older males. Our findings provide new insight into the mechanisms governing heat loss responses and suggest that the age‐related diminished COX‐dependent heat loss responses reported in previous studies may be a result of the reduced COX‐derived production of prostanoids (e.g., prostacyclin) rather than the decreased sensitivity of prostanoid receptors.