Administration of prostacyclin modulates cutaneous blood flow but not sweating in young and older males: roles for nitric oxide and KCa channels

Abstract

Cyclooxygenase (COX) contributes to the regulation of cutaneous vasodilatation and sweating; however the mechanism(s) underpinning this response remains 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, since ageing attenuates COX-dependent cutaneous vasodilatation and sweating. In young (25 ± 4 years) and older (60 ± 6 years) males (9 per group), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm skin sites: 1) Control, 2) 10 mm l-NNA, a non-specific NOS inhibitor, 3) 50 mm tetraethylammonium (TEA), a non-specific KCa channel blocker, and 4) 10 mm l-NNA + 50 mm TEA. All fours sites were co-administered with prostacyclin in an incremental manner (0.04, 0.4, 4, 40, 400 μm each for 25 min). Prostacyclin-induced increases in CVC were similar between groups (all concentrations, P > 0.05). l-NNA and TEA and 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), and 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 while prostacyclin does not mediate sweating, it modulates cutaneous vasodilatation to a similar extent in young and older males. Further, while 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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