Female C57BL/6J mice lacking the circadian clock protein PER1 are protected from nondipping hypertension

Nov 15, 2018American journal of physiology. Regulatory, integrative and comparative physiology

Female mice missing the clock protein PER1 may be protected from high blood pressure that doesn’t drop at night

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Abstract

Loss of the circadian clock protein PER1 in female mice does not significantly change mean arterial pressure or blood pressure rhythm.

A high-salt diet combined with deoxycorticosterone pivalate treatment resulted in increased mean arterial pressure in both female Per1-knockout and wild-type mice.
Both genotypes maintained a greater than 10% dip in blood pressure, unlike the nondipping hypertension observed in male Per1-knockout mice.
The absence of significant changes in blood pressure regulation in female Per1-knockout mice suggests a protective mechanism associated with female sex.
These findings indicate that the role of PER1 in blood pressure regulation may differ between sexes.

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The circadian clock is integral to the maintenance of daily rhythms of many physiological outputs, including blood pressure. Our laboratory has previously demonstrated the importance of the clock protein period 1 (PER1) in blood pressure regulation in male mice. Briefly, a high-salt diet (HS; 4% NaCl) plus injection with the long-acting mineralocorticoid deoxycorticosterone pivalate (DOCP) resulted in nondipping hypertension [<10% difference between night and day blood pressure (BP) in Per1-knockout (KO) mice but not in wild-type (WT) mice]. To date, there have been no studies that have examined the effect of a core circadian gene KO on BP rhythms in female mice. The goal of the present study was to determine whether female Per1-KO mice develop nondipping hypertension in response to HS/DOCP treatment. For the first time, we demonstrate that loss of the circadian clock protein PER1 in female mice does not significantly change mean arterial pressure (MAP) or the BP rhythm relative to female C57BL/6 WT control mice. Both WT and Per1-KO female mice experienced a significant increase in MAP in response to HS/DOCP. Importantly, however, both genotypes maintained a >10% dip in BP on HS/DOCP. This effect is distinct from the nondipping hypertension seen in male Per1-KO mice, demonstrating that the female sex appears to be protective against PER1-mediated nondipping hypertension in response to HS/DOCP. Together, these data suggest that PER1 acts in a sex-dependent manner in the regulation of cardiovascular rhythms.

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Female C57BL/6J mice lacking the circadian clock protein PER1 are protected from nondipping hypertension

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