Abstract
Activation of central chemoreceptors by CO2 increases BP, sympathetic nerve activity (SNA), and breathing. Experiments using SHRs, a well‐established neurogenic hypertensive model, have shown that the high BP is associated with elevated SNA and peripheral chemoreflexes, and an impaired baroreflex. Earlier we showed that adult SHRs have enhanced ventilatory (VE) and BP responses to hypercapnia, and blocking both orexin receptors can normalize such enhanced responses and markedly lower BP. Here, using juvenile SHRs (P42‐60), we report that: 1) VE responses to normoxic‐hypercapnia and hyperoxic‐hypercapnia (179±25 & 162±38 %increase respectively) are higher than that of age‐matched normal rats (118±22 & 113±26 %increase, respectively), but lower than that of adult SHRs (226±39 % increase)(P<0.05); 2) resting BP is higher than of age‐matched normal rats (130±12 & 99±5mmHg respectively), but lower than that of adult SHRs (157±12mmHg)(P<0.05). Summary, in SHRs 1) significant increases in both CO2 chemoreflex and BP are measureable in juveniles; 2) the enhanced CO2 chemoreflex persists while peripheral chemoreceptors were inhibited by hyperoxia indicate an important role for central chemoreflex in neurogenic hypertension. We suggest that the enhanced CO2 chemoreflex in early life may be causally linked to the development of neurogenic hypertension in SHRs, and modulation of the overactive CO2 chemoreflex could be beneficial in treating neurogenic hypertension. (HL 28066)
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