ArticleProceedings of the National Academy of Sciences of the United States of America2009
Hypertension of Kcnmb1-/- is linked to deficient K secretion and aldosteronism.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 100 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Osmolarity Controls Oscillatory Calcium Signaling to Reduce Autonomous Aldosterone Production in Zona Glomerulosa Cells.Endocrinology · 2025Article
- Diet-Microbiota-Host Interactions in Regulation of Cardiometabolic Homeostasis: Emerging Mechanisms and Therapeutic Potential.Microbiota and host · 2025Article
- Identification and validation of prognostic genes and prognostic models associated with cutaneous melanoma and integrative stress response.Frontiers in immunology · 2025Article
- Going with the flow: New insights regarding flow induced KPhysiological reports · 2024Review
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- TRPV4 expression in the renal tubule is necessary for maintaining whole body KAmerican journal of physiology. Renal physiology · 2023Article
- Differential Functional Contribution of BK Channel Subunits to Aldosterone-Induced Channel Activation in Vascular Smooth Muscle and Eventual Cerebral Artery Dilation.International journal of molecular sciences · 2023Article
- Aldosterone: Renal Action and Physiological Effects.Comprehensive Physiology · 2023Article
- The function of BK channels extracted and purified within SMALPs.The Biochemical journal · 2022Article
- With-No-Lysine Kinase 1 (WNK1) Augments TRPV4 Function in the Aldosterone-Sensitive Distal Nephron.Cells · 2021Article
- Ion Channel Function and Electrical Excitability in the Zona Glomerulosa: A Network Perspective on Aldosterone Regulation.Annual review of physiology · 2021Review
- Calcium-Activated KHandbook of experimental pharmacology · 2021Article
- Effects of extreme potassium stress on blood pressure and renal tubular sodium transport.American journal of physiology. Renal physiology · 2020Article
- Chemogenetic activation of adrenocortical Gq signaling causes hyperaldosteronism and disrupts functional zonation.The Journal of clinical investigation · 2020Article
- Regulation of BK Channels by Beta and Gamma Subunits.Annual review of physiology · 2019Review
- Beneficial Effects of High Potassium: Contribution of Renal Basolateral KHypertension (Dallas, Tex. : 1979) · 2018Review
- Mouse Models of Primary Aldosteronism: From Physiology to Pathophysiology.Endocrinology · 2017Article
- Association between potassium channel SNPs and essential hypertension in Xinjiang Kazak Chinese patients.Experimental and therapeutic medicine · 2017Article
- The renal TRPV4 channel is essential for adaptation to increased dietary potassium.Kidney international · 2017Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Mice lacking the beta1-subunit (gene, Kcnmb1; protein, BK-beta1) of the large Ca-activated K channel (BK) are hypertensive. This phenotype is thought to result from diminished BK currents in vascular smooth muscle where BK-beta1 is an ancillary subunit. However, the beta1-subunit is also expressed in the renal connecting tubule (CNT), a segment of the aldosterone-sensitive distal nephron, where it associates with BK and facilitates K secretion. Because of the correlation between certain forms of hypertension and renal defects, particularly in the distal nephron, it was determined whether the hypertension of Kcnmb1(-/-) has a renal origin. We found that Kcnmb1(-/-) are hypertensive, volume expanded, and have reduced urinary K and Na clearances. These conditions are exacerbated when the animals are fed a high K diet (5% K; HK). Supplementing HK-fed Kcnmb1(-/-) with eplerenone (mineralocorticoid receptor antagonist) corrected the fluid imbalance and more than 70% of the hypertension. Finally, plasma [aldo] was elevated in Kcnmb1(-/-) under basal conditions (control diet, 0.6% K) and increased significantly more than wild type when fed the HK diet. We conclude that the majority of the hypertension of Kcnmb1(-/-) is due to aldosteronism, resulting from renal potassium retention and hyperkalemia.
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