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

摘要

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 (254years) and older (606years) males (nine per group), cutaneous vascular conductance (CVC) and sweat rate were evaluated at four intradermal forearm skin sites: (i) control; (ii) 10mmN(G)-nitro-l-arginine (l-NNA), a non-specific NOS inhibitor; (iii) 50mm tetraethylammonium (TEA), a non-specific KCa channel blocker; and (iv) 10mm l-NNA + 50mm TEA. All four sites were coadministered with prostacyclin in an incremental manner (0.04, 0.4, 4, 40 and 400m each for 25min). 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 (P0.05), with the exception of l-NNA at 0.04m (P>0.05). In older males, CVC during prostacyclin administration was not influenced by l-NNA (all concentrations), TEA (4-400m) or their combination (400m) (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.