K channels are major contributors to ATP-induced cutaneous vasodilation in healthy older adults.

Objective: To examine the contributions of calcium-activated K (K) channels and nitric oxide synthase (NOS) to adenosine triphosphate (ATP)-induced cutaneous vasodilation in healthy older adults.

Methods: In eleven older adults (69 ± 2 years, 5 females), cutaneous vascular conductance, normalized to maximum vasodilation (%CVC) was assessed at four dorsal forearm skin sites that were continuously perfused with either 1) lactated Ringer solution (Control), 2) 50 mM tetraethylammonium (TEA, K channel blocker), 3) 10 mM N-nitro-L-arginine (L-NNA, NOS inhibitor), or 4) combined 50 mM TEA +10 mM L-NNA, via microdialysis. Local skin temperature was fixed at 33 °C at all sites with local heaters throughout the protocol while the cutaneous vasodilator response was assessed during coadministration of ATP (0.

Heat shock protein 90 modulates cutaneous vasodilation during an exercise-heat stress, but not during passive whole-body heating in young women.

Heat shock protein 90 (HSP90) modulates exercise-induced cutaneous vasodilation in young men via nitric oxide synthase (NOS), but only when core temperature is elevated ~1.0°C. While less is known about modulation of this heat loss response in women during exercise, sex differences may exist.

Regional influence of nitric oxide on cutaneous vasodilatation and sweating during exercise-heat stress in young men.

New Findings: What is the central question of this study? Do regional differences exist in nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and sweating during exercise-heat stress in young men. What is the main finding and its importance? Exercise-induced increases in cutaneous vasodilatation and sweating were greater on the chest and upper back compared to the forearm, although the NOS contribution to cutaneous vasodilatation was similar across all regions. Conversely, there was a greater NOS-dependent rate of change in sweating on the chest compared to the forearm, with a similar trend on the back.

Intradermal Administration of Atrial Natriuretic Peptide Attenuates Cutaneous Vasodilation but Not Sweating in Young Men during Exercise in the Heat.

Introduction: Prolonged exercise in the heat stimulates plasma release of atrial natriuretic peptide (ANP) in association with dehydration-induced reductions in blood volume. Elevated plasma ANP levels under these conditions may indirectly attenuate cutaneous blood flow and sweating responses due to the effects of this hormone on central blood volume and plasma osmolality and the resulting stimulation of nonthermal reflexes. However, it remains unclear whether cutaneous blood flow and sweating are directly modulated by ANP at the level of the cutaneous end organs (cutaneous microvessels and eccrine sweat glands) during prolonged exercise in the heat.

Whole-body heat exchange in black-African and Caucasian men during exercise eliciting matched heat-loss requirements in dry heat.

New Findings: What is the central question of this study? Black-African descendants are thought, by some, to possess genotypic adaptations conducive to survival in hot climates. We therefore assessed whether Canadian residents of black-African descent display enhanced whole-body total heat loss (evaporative plus dry heat exchange) in comparison to Caucasian Canadians during exercise eliciting matched heat-loss requirements in dry heat. What is the main finding and its importance? Neither whole-body total heat loss nor body heat storage differed significantly between groups, irrespective of the exercise intensity.

Contribution of nitric oxide synthase to cutaneous vasodilatation and sweating in men of black-African and Caucasian descent during exercise in the heat.

New Findings: What is the central question of this study? Nitric oxide modulates cutaneous vasodilatation and sweating during exercise-induced heat stress in young men. However, it remains uncertain whether these effects are reduced in black-African descendants, who commonly demonstrate reduced nitric oxide bioavailability. Therefore, we assessed whether black-African descendants display reduced nitric oxide-dependent cutaneous vasodilatation and sweating compared with Caucasians in these conditions.

Separate and combined effects of K and K channel blockade with NOS inhibition on cutaneous vasodilation and sweating in older men during heat stress.

Our objective in this study was to examine the separate and combined effects of potassium (K) channels and nitric oxide synthase (NOS) on cutaneous vasodilation and sweating in older men during rest and exercise in the heat. In 13 habitually active men (61 ± 4 yr), cutaneous vascular conductance and local sweat rate were assessed at six dorsal forearm skin sites continuously perfused with either ) lactated Ringer (control), ) 10 mM -nitro-l-arginine methyl ester (l-NAME, NOS inhibitor), ) 50 mM tetraethylammonium (TEA; Ca-activated K channel blocker), ) 5 mM glybenclamide (GLY; ATP-sensitive K channel blocker), ) 50 mM TEA + 10 mM l-NAME, and ) 5 mM GLY + 10 mM l-NAME via microdialysis. Participants rested in non-heat stress (25°C) and heat stress (35°C) conditions for ∼60 min each, followed by 50 min of moderate-intensity cycling (∼55% V̇o) and 30 min of recovery in the heat.

Heat shock protein 90 does not contribute to cutaneous vasodilatation in older adults during heat stress.

Objectives: Heat shock protein 90 (HSP90) contributes to cutaneous vasodilatation during exercise in the heat through nitric oxide (NO) synthase (NOS)-dependent mechanisms in young adults. We hypothesized that similar responses would be observed in older middle-aged adults.

Methods: In nineteen habitually active older middle-aged (56 ± 5 years) men (n = 9) and women (n = 10), cutaneous vascular conductance (CVC) was measured at four forearm skin sites continuously treated with (a) lactated Ringers solution (Control), (b) 10 mmol/L L-NAME (NOS inhibitor), (c) 178 μmol/L geldanamycin (HSP90 inhibitor), or (d) 10 mmol/L L-NAME and 178 μmol/L geldanamycin combined.