scholarly journals SP039HYPERTENSION-RELATED PROTEIN DEACETYLASE SIRT3 AFFECTS BLOOD PRESSURE THROUGH REGULATION OF INTESTINAL SALT ABSORPTION IN MICE

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Masaki Ryuzaki ◽  
Kazutoshi Miyashita ◽  
Masaaki Sato ◽  
Asuka Uto ◽  
Sho Endo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Related Protein ◽  
Salt Absorption ◽  
Protein Deacetylase

scholarly journals Knockdown of parathyroid hormone related protein in smooth muscle cells alters renal hemodynamics but not blood pressure

2013 ◽  
Vol 305 (3) ◽  
pp. F333-F342 ◽  
Author(s):  
Denis Raison ◽  
Catherine Coquard ◽  
Mazène Hochane ◽  
Jacques Steger ◽  
Thierry Massfelder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Parathyroid Hormone ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Renal Plasma Flow ◽  
Renal Hemodynamics ◽  
Related Protein ◽  
Filtration Fraction ◽  
Parathyroid Hormone Related Protein

Parathyroid hormone-related protein (PTHrP) belongs to vasoactive factors that regulate blood pressure and renal hemodynamics both by reducing vascular tone and raising renin release. PTHrP is expressed in systemic and renal vasculature. Here, we wanted to assess the contribution of vascular smooth muscle cell endogenous PTHrP to the regulation of cardiovascular and renal functions. We generated a mouse strain ( SMA-CreER T2/ PTHrP L2/L2 or premutant PTHrP SM−/−), which allows temporally controlled, smooth muscle-targeted PTHrP knockdown in adult mice. Tamoxifen treatment induced efficient recombination of PTHrP-floxed alleles and decreased PTHrP expression in vascular and visceral smooth muscle cells of PTHrP SM−/− mice. Blood pressure remained unchanged in PTHrP SM−/− mice, but plasma renin concentration and creatinine clearance were reduced. Renal hemodynamics were further analyzed during clearance measurements in anesthetized mice. Conditional knockdown of PTHrP decreased renal plasma flow and glomerular filtration rate with concomitant reduction in filtration fraction. Similar measurements were repeated during acute saline volume expansion. Saline volume expansion induced a rise in renal plasma flow and reduced filtration fraction; both were blunted in PTHrP SM−/− mice leading to impaired diuresis. These findings show that endogenous vascular smooth muscle PTHrP controls renal hemodynamics under basal conditions, and it is an essential factor in renal vasodilation elicited by saline volume expansion.

scholarly journals C1q/TNF-α–Related Protein 1 (CTRP1) Maintains Blood Pressure Under Dehydration Conditions

2018 ◽  
Vol 123 (5) ◽  
Author(s):  
Sora Han ◽  
Ae Lee Jeong ◽  
Sunyi Lee ◽  
Jeong Su Park ◽  
Sumiyasuren Buyanravjikh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Related Protein ◽  
Tnf Α

scholarly journals The TRPA1 channel is a cardiac target of mIGF-1/SIRT1 signaling

2014 ◽  
Vol 307 (7) ◽  
pp. H939-H944 ◽  
Author(s):  
Valerio Pazienza ◽  
Cristoforo Pomara ◽  
Francesco Cappello ◽  
Raffaele Calogero ◽  
Matteo Carrara ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Sirtuin 1 ◽  
Cardiovascular Stress ◽  
Hormetic Effect ◽  
Dependent Protein ◽  
Transient Receptor ◽  
Protein Deacetylase ◽  
Acting Muscle

Cardiac overexpression of locally acting muscle-restricted (m)IGF-1 and the consequent downstream activation of NAD+-dependent protein deacetylase sirtuin 1 (SIRT1) trigger potent cardiac antioxidative and antihypertrophic effects. Transient receptor potential (TRP) cation channel A1 (TRPA1) belongs to the TRP ion channel family of molecular detectors of thermal and chemical stimuli that activate sensory neurons to produce pain. Recently, it has been shown that TRPA1 activity influences blood pressure, but the significance of TRPA1 in the cardiovascular system remains elusive. In the present work, using genomic screening in mouse hearts, we found that TRPA1 is a target of mIGF-1/SIRT1 signaling. TRPA1 expression is increased in the heart of cardiac-restricted mIGF-1 transgenic (Tg) mice, both in cardiomyocytes and noncardiomyocytes. In wild-type mice, SIRT1 occupied the TRPA1 promoter, inhibiting its expression, whereas in the presence of the cardiac mIGF-1 transgene, SIRT1 was displaced from the TRPA1 promoter, leading to an increase in its expression. Cardiac-specific ablation of SIRT1 (cardiac-specific knockout) in mIGF-1 Tg mice paradoxically did not increase TRPA1 expression. We have recently reported a systemic “hormetic” effect in mIGF-1 Tg mice, mild hypertension, which was depleted upon cardiac-specific knockout of SIRT1. Administration of the selective TRPA1 antagonist HC-030031 to mIGF-1 Tg mice restored blood pressure to basal levels. We identified TRPA1 as a functional target of the cardiac mIGF-1/SIRT1 signaling pathway, which may have pharmacological implications for the management of cardiovascular stress.

scholarly journals A novel blood pressure modulator C1q/TNF-α-related protein 1 (CTRP1)

BMB Reports ◽  
2018 ◽  
Vol 51 (12) ◽  
pp. 611-612 ◽  
Author(s):  
Sora Han ◽  
Young Yang
Keyword(s):  
Blood Pressure ◽  
Related Protein ◽  
Tnf Α

Abstract P160: C1q/TNF-related Protein 1 Induces Obesity-related Hypertension In Mice Via Renal Na+ Retention In The Proximal Tubules

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Fei Wang ◽  
Huaqing Zheng ◽  
Renfei Luo ◽  
Tianxin Yang
Keyword(s):  
Blood Pressure ◽  
Urinary Sodium Excretion ◽  
Vehicle Group ◽  
Related Protein ◽  
Plasma Volume Expansion ◽  
Urine Albumin ◽  
Diet Induced Obesity ◽  
Diabetes And Obesity

A recently identified adipokine C1q/TNF-related protein 1 (CTRP1) displayed a potent beneficial effect in managing metabolic disorders during type 2 diabetes and obesity. However, little is known about a potential role of CTRP1 in regulation of renal function and blood pressure (BP) in the context of obesity. Therefore, the present study aimed to determine the effect of a recombinant CTRP1 protein (termed CTRP1-His) on blood pressure in mice with diet-induced obesity (DIO). 8-mo-old male C57/B6 mice were fed a high-fat diet (60 Kcal% fat) for eight weeks and were infused with vehicle or CTRP1-His (10 ng/min/kg) via subcutaneously implanted osmotic minipump for the last seven days. BP parameters were recorded using telemetry devices. Consistent with other groups’ studies, mice infused with CTRP1-His exhibited remarkably improved multiple metabolic parameters, including hyperglycemia and hyperinsulinemia. Compared to the vehicle group, BP responses to CTRP1-His treatment developed a modest but significant increase in BP (MAP on day 7 [mmHg]: 122.3 ± 2.2 vs. 109 ± 1.73, n = 3 per each group, p < 0.01) accompanied with decreased hematocrit (Hct [%]: 43.8 ± 1.3 vs. 49 ± 1.2 %, p < 0.05), an index of plasma volume expansion. The DIO mice infused with CTRP1-His demonstrated a reduced urinary sodium excretion (U Na /Creatinine [mmol/mg]: 0.17 ± 0.04 vs. 0.27 ± 0.06, p = 0.07). By immunoblotting CTRP1-His infusion induced significant upregulation of renal abundances of p-NHE3, V2R, and AQP2 but suppressed obesity-induced renal abundances of p-NCC/NCC, p-NKCC2/NKCC2, and cleaved α-ENaC protein. Interestingly, CTRP1-His infusion tends to decrease albuminuria (urine albumin/Creatinine [mg/g]: 78.8 ± 7.7 vs. 120.5 ± 14, p = 0.07) in the DIO mice. Overall, our results indicated that CTRP1-His exerted a pressor effect in DIO mice via stimulating sodium-water retention through activation of NHE3 and AQP2 associated with compensatory attenuation of Na+ transporters in the distal nephron.

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