Administration of prostacyclin modulates cutaneous bloodflow but not sweating in young and older males: roles for nitric oxide and calcium-activated potassium channels
Cyclooxygenase (COX) contributes to the regulation of cutaneous vasodilatation and sweating; however, the mechanism(s) underpinning this response remain unresolved. We hypothesized that prostacyclin (a COX-derived product) may directly mediate cutaneous vasodilatation and sweating through nitric oxide synthase (NOS) and calcium-activated potassium (KCa) channels in young adults. However, these responses would be diminished in older adults because ageing attenuates COX-dependent cutaneous vasodilatation and sweating. In young (25 ± 4 years) and older (60 ± 6 years) males (nine per group), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm skin sites: (i) control; (ii) 10 mM NG-nitro-L-arginine (L-NNA), a non-specific NOS inhibitor; (iii) 50 mM tetraethylammonium (TEA), a non-specific KCa channel blocker; and (iv) 10 mM L-NNA + 50 mM TEA. All four sites were coadministered with prostacyclin in an incremental manner (0.04, 0.4, 4, 40 and 400 μM each for 25 min). Prostacyclin-induced increases in CVC were similar between groups (all concentrations, P > 0.05). L-NNA and TEA, as well as their combination, lowered CVC in young males at all prostacyclin concentrations (P 0.05), with the exception of L-NNA at 0.04 μM (P > 0.05). In older males, CVC during prostacyclin administration was not influenced by L-NNA (all concentrations), TEA (4-400 μM) or their combination (400 μM) (P > 0.05). No effect on sweat rate was observed in either group (all concentrations, P > 0.05). We conclude that, although prostacyclin does not mediate sweating, it modulates cutaneous vasodilatation to a similar extent in young and older males. Furthermore, although NOS and KCa channels contribute to the prostacyclin-induced cutaneous vasodilatation in young males, these contributions are diminished in older males.
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