ArticleJournal of the American Society of Nephrology : JASN2000
Exaggerated impact of ATP-sensitive K(+) channels on afferent arteriolar diameter in diabetes mellitus.
Article in Journal of the American Society of Nephrology : JASN, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 56 citations in OpenAlex.
- Ion channels and transporters in diabetic kidney disease.Current topics in membranes · 2019Review
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- NGS nominated CELA1, HSPG2, and KCNK5 as candidate genes for predisposition to Balkan endemic nephropathy.BioMed research international · 2014Article
- Role of GLUT4 on angiotensin 2-induced systemic and renal hemodynamics.Journal of experimental pharmacology · 2013Article
- Pharmacological targets in the renal peritubular microenvironment: implications for therapy for sepsis-induced acute kidney injury.Pharmacology & therapeutics · 2012Review
- Tempol prevents altered K(+) channel regulation of afferent arteriolar tone in diabetic rat kidney.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Closure of multiple types of K+ channels is necessary to induce changes in renal vascular resistance in vivo in rats.Pflugers Archiv : European journal of physiology · 2011Article
- Pathophysiology of the diabetic kidney.Comprehensive Physiology · 2011Review
- The renal vascular response to diabetes.Current opinion in nephrology and hypertension · 2010Review
- C-Peptide: the missing link in diabetic nephropathy?The review of diabetic studies : RDS · 2009Article
- Renal and vascular benefits of C-peptide: Molecular mechanisms of C-peptide action.Biologics : targets & therapy · 2008Article
- K(ATP)-mediated vasodilation is impaired in obese Zucker rats.Microcirculation (New York, N.Y. : 1994) · 2008Article
- Potassium channel contributions to afferent arteriolar tone in normal and diabetic rat kidney.American journal of physiology. Renal physiology · 2008Article
- Insulin induces the release of vasodilator compounds from platelets by a nitric oxide-G kinase-VAMP-3-dependent pathway.The Journal of experimental medicine · 2004Article
- Kv channel subunits that contribute to voltage-gated K+ current in renal vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2003Article
- Tyrosine kinase involvement in renal arteriolar constrictor responses to angiotensin II.Hypertension (Dallas, Tex. : 1979) · 2001Article
- Altered electromechanical coupling in the renal microvasculature during the early stage of diabetes mellitus.Clinical and experimental pharmacology & physiologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Experiments were performed to determine the involvement of ATP-sensitive K(+) channels (K(ATP) channels) in the renal afferent arteriolar dilation that occurs during the hyperfiltration stage of insulin-dependent diabetes mellitus (IDDM). IDDM was induced in rats by streptozotocin (STZ) injection, and adequate insulin was provided to maintain moderate hyperglycemia. Sham rats received vehicle treatments. Two weeks later, afferent arteriolar function was assessed using the in vitro blood-perfused juxtamedullary nephron technique. Baseline afferent arteriolar lumen diameter was greater in STZ rats (25.9 +/- 1.1 microm) than in sham rats (20.8 +/- 1.0 microm). Glibenclamide (3 to 300 microM) had virtually no effect on afferent arterioles from sham rats; however, this K(ATP) antagonist caused concentration-dependent afferent arteriolar constriction in kidneys from STZ-treated rats, restoring lumen diameter to 20.6 +/- 1.7 microm (P > 0.05 versus sham baseline). In both groups of rats, pinacidil (a cyanoguanidine K(ATP) agonist; 0.3 to 300 microM) evoked concentration-dependent afferent arteriolar dilation, indicating the functional expression of K(ATP) channels; however, lumen diameter was increased by 73% in STZ kidneys but only by 48% in sham kidneys. The gliben-clamide-sensitive afferent arteriolar dilator response to 1 microM PCO-400 (a benzopyran K(ATP) agonist) was also accentuated in STZ kidneys. These observations suggest that increases in both the functional availability and basal activation of K(ATP) channels promote afferent arteriolar vasodilation during the early stage of IDDM, changes that likely contribute to the etiology of diabetic hyperfiltration.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.