Atrial natriuretic peptide (ANP) increases during exercise in the heat wherein heat loss responses of sweating and cutaneous vasodilatation are activated. Hence ANP might be involved in the regulation of sweating and cutaneous vasodilatation. However, whether ANP directly mediates sweating and cutaneous vasodilatation needs to be clarified. Also, muscarinic receptor activation induces sweating and cutaneous vasodilatation, however, it remains to be determined whether ANP modulates these responses. In this study, in 11 young males (25 ± 5 years), cutaneous vascular conductance and sweat rate were assessed at intradermal microdialysis sites that were continuously perfused with either lactated Ringer (Control) or 3 different concentrations of ANP (0.1, 1, 10 µM). All 4 sites were co-administrated with methacholine, a muscarinic receptor agonist, in a dose-dependent fashion (0.0125, 0.25, 5, 100, and 2000 mM, 25 min for each). ANP at all concentrations did not increase sweat rate and cutaneous vascular conductance as compared with pre-ANP infusion values (all P > 0.05). Methacholine increased both sweat rate and cutaneous vascular conductance (all P ≤ 0.05). However, the responses were unaffected by co-administration of ANP relative to methacholine only, even as assessed in context of the methacholine concentration required to elicit 50% of the maximal response (EC50) (all P > 0.05). We show that exogenous ANP administration intradermally does not directly modulate sweating and cutaneous vasodilatation under room temperature conditions in resting young adults. Further, there is no effect of ANP on muscarinic sweating and cutaneous vasodilatation.
Keywords: heat loss responses; microcirculation; thermoregulation.