ArticleMolecular pharmacology2008
Sulfonylurea receptor-dependent and -independent pathways mediate vasodilation induced by ATP-sensitive K+ channel openers.
Article in Molecular pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Potassium channel-targeted therapy in reducing vascular complications in diabetes mellitus: novel insights.Frontiers in pharmacology · 2026Review
- Pulmonary hypertension associated with diazoxide: the SUR1 paradox.ERJ open research · 2023Review
- Diazoxide affects mitochondrial bioenergetics by the opening of mKATP channel on submicromolar scale.BMC molecular and cell biology · 2020Article
- The expression of KAnnals of translational medicine · 2018Article
- Reassessment of risk genotypes (GRN, TMEM106B, and ABCC9 variants) associated with hippocampal sclerosis of aging pathology.Journal of neuropathology and experimental neurology · 2015Article
- Eugenol dilates rat cerebral arteries by inhibiting smooth muscle cell voltage-dependent calcium channels.Journal of cardiovascular pharmacology · 2014Article
- Diversity of mitochondria-dependent dilator mechanisms in vascular smooth muscle of cerebral arteries from normal and insulin-resistant rats.American journal of physiology. Heart and circulatory physiology · 2014Article
- Direct activation of β-cell KATP channels with a novel xanthine derivative.Molecular pharmacology · 2014Article
- Smooth muscle cell transient receptor potential polycystin-2 (TRPP2) channels contribute to the myogenic response in cerebral arteries.The Journal of physiology · 2013Article
- The voltage-dependent L-type Ca2+ (CaV1.2) channel C-terminus fragment is a bi-modal vasodilator.The Journal of physiology · 2013Article
- Transcriptional upregulation of α2δ-1 elevates arterial smooth muscle cell voltage-dependent Ca2+ channel surface expression and cerebrovascular constriction in genetic hypertension.Hypertension (Dallas, Tex. : 1979) · 2012Article
- Hydrogen sulfide activates Ca²⁺ sparks to induce cerebral arteriole dilatation.The Journal of physiology · 2012Article
- Vasodilation induced by oxygen/glucose deprivation is attenuated in cerebral arteries of SUR2 null mice.American journal of physiology. Heart and circulatory physiology · 2011Article
- Hydrogen sulfide dilates cerebral arterioles by activating smooth muscle cell plasma membrane KATP channels.American journal of physiology. Heart and circulatory physiology · 2011Article
- Ca(V)1.2 channel N-terminal splice variants modulate functional surface expression in resistance size artery smooth muscle cells.The Journal of biological chemistry · 2011Article
- Caveolin-1 assembles type 1 inositol 1,4,5-trisphosphate receptors and canonical transient receptor potential 3 channels into a functional signaling complex in arterial smooth muscle cells.The Journal of biological chemistry · 2011Article
- Hydrogen sulfide and cerebral microvascular tone in newborn pigs.American journal of physiology. Heart and circulatory physiology · 2011Article
- Persistent hyperinsulinemic hypoglycemia of infancy: constitutive activation of the mTOR pathway with associated exocrine-islet transdifferentiation and therapeutic implications.International journal of clinical and experimental pathology · 2010Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
ATP-sensitive K+ (KATP) channel openers are vasodilators that activate both plasma membrane and mitochondrial KATP channels. Here, we investigated the molecular mechanisms by which diazoxide and pinacidil induce vasodilation by studying diameter regulation of wild-type [SUR2(+/+)] and sulfonylurea receptor (SUR) 2-deficient [SUR2(-/-)] mouse myogenic mesenteric arteries. Ryanodine (10 microM), a ryanodine-sensitive Ca2+ release (RyR) channel blocker; iberiotoxin (100 nM), a large-conductance Ca2+-activated K+ (KCa) channel blocker; 4-aminopyridine (4-AP; 1 mM), a voltage-gated K+ (KV) channel blocker; manganese(III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP; 100 microM), an antioxidant; and a combination of ryanodine and 4-AP reduced diazoxide (100 microM)-induced dilation in pressurized (60 mm Hg) SUR2(+/+) arteries by 45 to 77%. In contrast, these inhibitors did not alter pinacidil (5 microM)-induced dilation in SUR2(+/+) arteries. Reverse transcription-polymerase chain reaction indicated that SUR2B was the only SUR isoform expressed in SUR2(+/+) mesenteric artery smooth muscle cells, whereas SURs were absent in SUR2(-/-) cells. In SUR2(-/-) arteries, pinacidil-induced vasodilation was 10% of that in SUR2(+/+) arteries, whereas diazoxide-induced vasodilation was similar in SUR2(+/+) and SUR2(-/-) arteries. Atpenin (1 microM), a selective electron transport chain (ETC) complex II inhibitor, dilated arteries similarly to diazoxide, and this effect was attenuated by MnTMPyP and ryanodine + 4-AP. Atpenin also attenuated diazoxide-, but not pinacidil-induced vasodilation. In summary, data indicate that pinacidil-induced vasodilation requires SUR2B, whereas diazoxide-induced vasodilation does not require SURs. Rather, diazoxide-induced vasodilation involves ETCII inhibition; a smooth muscle cell-reactive oxygen species elevation; and RyR, KCa, and KV channel activation. These data indicate that KATP channel openers regulate arterial diameter via SUR-dependent and -independent pathways.
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Registered trials
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