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C1q/TNF-α-Related Protein 1 (CTRP1) Maintains Blood Pressure Under Dehydration Conditions
Sora Han1, Ae Lee Jeong2, Sunyi Lee3
1From the Research Institute of Women's Health (S.H.).
Insights
C1q/TNF-α-related protein 1 (CTRP1) helps maintain normal blood pressure (BP) during dehydration. Impaired CTRP1 function can lead to hypertension, highlighting its role in BP regulation.
Area of Science:
- Endocrinology
- Cardiovascular Physiology
- Molecular Biology
Background:
- Circulating C1q/TNF-α-related protein 1 (CTRP1) levels are elevated in hypertensive individuals.
- The precise role of CTRP1 in blood pressure (BP) regulation remains largely unelucidated.
Purpose of the Study:
- To elucidate the physiological and pathophysiological functions of CTRP1 in BP homeostasis.
- To investigate CTRP1's role in preventing dehydration-induced hypotension.
Main Methods:
- Utilized inducible CTRP1 knockout (CTRP1ΔCAG) mice and CTRP1 transgenic (CTRP1 TG) mice.
- Investigated the role of glucocorticoids and AT1R signaling in CTRP1-mediated BP regulation.
- Examined CTRP1's effect on the AT1R-Rho/ROCK pathway and AT1R trafficking via AKT/AS160 phosphorylation.
Main Results:
- CTRP1 production increased to maintain normotension during dehydration, a function impaired in CTRP1ΔCAG mice.
- Glucocorticoids mediate CTRP1 upregulation under dehydration; mifepristone blocked this increase and attenuated BP recovery.
- CTRP1 promotes vasoconstriction by stimulating the AT1R-Rho/ROCK pathway and enhancing AT1R plasma membrane trafficking.
- Losartan administration reversed the hypertensive phenotype in CTRP1 TG mice.
Conclusions:
- CTRP1 plays a critical role in BP homeostasis by preventing dehydration-induced hypotension.
- CTRP1's mechanism involves the AT1R-Rho/ROCK pathway and glucocorticoid regulation.
Rationale:
Circulating CTRP1 (C1q/TNF-α [tumor necrosis factor-α]-related protein 1) levels are increased in hypertensive patients compared with those in healthy subjects. Nonetheless, little is known about the molecular and physiological function of CTRP1 in blood pressure (BP) regulation.
Objective:
To investigate the physiological/pathophysiological role of CTRP1 in BP regulation.
Methods And Results:
CTRP1 production was increased to maintain normotension under dehydration conditions, and this function was impaired in inducible CTRP1 KO (knockout) mice (CTRP1 ΔCAG). The increase in CTRP1 under dehydration conditions was mediated by glucocorticoids, and the antagonist mifepristone prevented the increase in CTRP1 and attenuated BP recovery. Treatment with a synthetic glucocorticoid increased the transcription, translation, and secretion of CTRP1 from skeletal muscle cells. Functionally, CTRP1 increases BP through the stimulation of the AT1R (Ang II [angiotensin II] receptor 1)-Rho (Ras homolog gene family)/ROCK (Rho kinase)-signaling pathway to induce vasoconstriction. CTRP1 promoted AT1R plasma membrane trafficking through phosphorylation of AKT and AKT substrate of 160 kDa (AS160). In addition, the administration of an AT1R blocker, losartan, recovered the hypertensive phenotype of CTRP1 TG (transgenic) mice.
Conclusions:
For the first time, we provide evidence that CTRP1 contributes to the regulation of BP homeostasis by preventing dehydration-induced hypotension.
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