Pituitary adenylate cyclase-activating polypeptide drives cardiorespiratory responses to heat stress in neonatal mice

The neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) has emerged as a principal and rate-limiting regulator of physiological stress responses in adult rodents and has been implicated in sudden infant death syndrome (SIDS). Recent studies show that PACAP plays a role in neonatal cardiorespiratory responses to hypoxia, hypercapnia, and hypothermia, but not hyperthermia, which is often associated with SIDS. Here we tested the hypothesis that, consistent with a role in SIDS, PACAP is involved in regulating the neonatal cardiorespiratory responses to severe heat. To address this, we used head-out plethysmography and surface ECG electrodes to study the cardiorespiratory physiology of conscious neonatal PACAP-null and wild-type mice at ambient temperatures of 32°C (baseline) and 40°C (heat stress). We also assessed body surface temperature as an indicator of cutaneous heat loss. Our results show that wild-type neonatal mice respond to heat stress by increasing ventilation (P = 0.007) and associated expired CO2 (P = 0.041), heart rate (P < 0.001), and cutaneous heat loss (P < 0.001). In PACAP-null neonates, this heat response is impaired, as indicated by a decrease in ventilation (P = 0.04) and associated expired CO2 (P = 0.006) and a blunted increase in heart rate (P = 0.001) and cutaneous heat loss (P = 0.0002). In addition, heart rate variability at baseline was lower in PACAP-null neonates than wild-type controls (P < 0.01). These results s...
Source: AJP: Regulatory, Integrative and Comparative Physiology - Category: Physiology Authors: Tags: Research Article Source Type: research