Critical role of striatin in blood pressure and vascular responses to dietary sodium intake
Open accessAbstract
Striatin is a protein regulator of vesicular trafficking in neurons that also binds caveolin-1 and Ca(2+)-calmodulin and could activate endothelial nitric oxide synthase. We have shown that striatin colocalizes with the mineralocorticoid receptor and that mineralocorticoid receptor activation increases striatin levels in vascular cells. To test whether striatin is a regulator of vascular function, wild-type and heterozygous striatin-deficient mice (Strn(+/-)) were randomized in crossover intervention to restricted (0.03%) and liberal sodium (1.6%) diets for 7 days on each diet, and blood pressure and aortic vascular function were measured. Compared with wild-type, sodium restriction significantly reduced blood pressure in Strn(+/-). On liberal salt intake, phenylephrine and high KCl caused a greater vascular contraction in Strn(+/-) than wild-type, and endothelium removal, nitric oxide synthase inhibitor L-NAME, and guanylate cyclase inhibitor ODQ enhanced phenylephrine contraction to a smaller extent in Strn(+/-) than wild-type. On liberal salt, acetylcholine relaxation was less in Strn(+/-) than in wild-type, and endothelium removal, L-NAME, and ODQ blocked acetylcholine relaxation, suggesting changes in endothelial NO-cGMP. On liberal salt, endothelial nitric oxide synthase mRNA expression and the ratio of endothelial nitric oxide synthase activator pAkt/total Akt were decreased in Strn(+/-) versus wild-type. Vascular relaxation to NO donor sodium nitroprusside was not different among groups. Thus, striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction, and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake.
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The blood pressure effects in STRN-deficient mice are in part due to changes in vascular contraction and relaxation, with increased aortic contraction upon phenylephrine or KCl and reduced relaxation upon acetylcholine.
“Additionally, the BP effects were in part due to changes in vascular contraction/relaxation, as an increased aortic contraction was observed upon phenylephrine or KCl addition, and a reduced aortic relaxation upon acetylcholine addition.”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [98]
Compared with wild-type, STRN-deficient mice show enhanced salt sensitivity of blood pressure, with a higher increase upon liberal salt intake and a higher decrease upon salt restriction.
“Compared with WT mice, STRN-deficient mice showed an enhanced salt sensitivity of their blood pressure (BP), characterized by a higher increase in BP upon liberal salt intake, and a higher decrease in BP upon salt restriction.”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [98]
Heterozygous mice for the PP2A B′′′ subunit STRN reveal a potential role for PP2A in the kidneys and blood pressure homeostasis.
“A potential role for PP2A in the kidneys and the regulation of blood pressure homeostasis was revealed in heterozygous mice for the PP2A B‴ subunit STRN [97,98].”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [98]
Endothelial NO and cGMP dampen the vascular sensitivity effects in STRN-deficient mice.
“In both cases, endothelial NO and cGMP dampened the vascular sensitivity effects [98].”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [98]
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- Authors
- Garza, A. E., Pojoga, L. H., Moize, B., Hafiz, W. M., Opsasnick, L. A., Siddiqui, W. T., Horenstein, M., Adler, G. K., Williams, G. H., & Khalil, R. A.
- Affiliations
- Brigham and Women's Hospital (US)
- ORCID
- Venue
- Hypertension
- Published
- 2015-09
- Volume
- 66
- Issue
- 3
- Pages
- 674-680
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC4537321
- OpenAlex
- W2108420936
- Cited by
- 31
- References
- 30
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 1 · 2021: 4 · 2020: 4 · 2019: 4 · 2018: 4 · 2017: 2 · 2016: 1 · 2015: 1
- FWCI
- 1.97
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL069208, HL-98724, R21HL111775, HL-104032, R01HL104032, HL 65998, R21HL098724, HL-69208, T32HL007609, R01HL114765, R01HL065998, R01HL144779, HL‐111775)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- striatin, salt sensitivity of blood pressure, sodium intake, mineralocorticoid receptor, endothelial nitric oxide synthase, nitric oxide/cGMP signaling, vascular function, vasoconstriction, vasorelaxation, acetylcholine, caveolin-1
- MeSH terms
- Animals, Aorta, Blood Pressure, Calmodulin-Binding Proteins, Enzyme Inhibitors, Cyclic GMP, Male, Membrane Proteins, Nerve Tissue Proteins, Phenylephrine, Sodium, Dietary, Vasoconstriction, Vasoconstrictor Agents, Mice, Knockout, NG-Nitroarginine Methyl Ester, Proto-Oncogene Proteins c-akt, Mice
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