Cardiorespiratory variability following repeat acute hypoxia in the conscious SHR versus two normotensive rat strains.

A link between exaggerated chemoreceptor sensitivity and hypertension has been documented in the spontaneously hypertensive rat (SHR) but has also been questioned when comparisons with normotensive strains other than the Wistar Kyoto (WKY) rat are made. To further evaluate the link between hypertension and chemoreflex sensitivity, changes in cardiorespiratory variability in response to three successive bouts of 5 min of hypoxia (21%→10%) were evaluated in conscious male SHR, and WKY and Sprague Dawley (SD) rats (n=7-8/group). In response to the first bout of hypoxia, the change in respiratory frequency (RF) was greatest in the SHR, but the increase in mean arterial pressure (MAP) was similar in both SHRs and WKY rats and all strains demonstrated a similar rise in heart rate (HR). All strains showed some level of response accommodation during subsequent bouts of hypoxia. Spectral analysis of HR variability identified a significant difference in high frequency (HF) power between strains during hypoxia, including an increase in HF power in the WKY rats, a decrease in the SHRs and little overall change in the SD rats. Alternatively, all strains demonstrated a rise in systolic arterial pressure (SAP) variability in the low frequency (LF) range in response to hypoxia but the increase was greatest in the SHR. Since SAP LF power is linked to vasosympathetic tone, these results support the hypothesis that essential hypertension is linked to exaggerated sympathetic responses to chemoreceptor stimulation but confirm that estimation of augmented reflex function cannot be determined by quantifying simple changes in MAP or HR.