ArticleInternational journal of molecular sciences2022
Sodium Nitroprusside-Induced Activation of Vascular Smooth Muscle BK Channels Is Mediated by PKG Rather Than by a Direct Interaction with NO.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Mechanisms Underlying the Biphasic Effects of Hydrogen Sulfide in Rat Intrapulmonary Arteries.Biomedicines · 2026Article
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- Microcirculatory responses at rest and during exercise in limited cutaneous systemic sclerosis compared to age-matched healthy adults.Frontiers in sports and active living · 2026Article
- Potassium channel-mediated NO-induced vasodilation during maturation: Dominance of Kv7 channels.FASEB bioAdvances · 2025Article
- Dual role of calcium-activated potassium channels of high conductance: facilitator or limiter of NO-induced arterial relaxation?Frontiers in physiology · 2025Article
- BK Channels in Tail Artery Vascular Smooth Muscle Cells of Normotensive (WKY) and Hypertensive (SHR) Rats Possess Similar Calcium Sensitivity But Different Responses to the Vasodilator Iloprost.International journal of molecular sciences · 2024Article
- Spreading depolarizations pose critical energy challenges in acute brain injury.Journal of neurochemistry · 2024Review
- Recent Developments in Ion Channel and Ion-Related Signaling.International journal of molecular sciences · 2023Article
- Article
- Activation of AMPK/miR-181b Axis Alleviates Endothelial Dysfunction and Vascular Inflammation in Diabetic Mice.Antioxidants (Basel, Switzerland) · 2022Article
- The Effects of Acidosis on eNOS in the Systemic Vasculature: A Focus on Early Postnatal Ontogenesis.International journal of molecular sciences · 2022Review
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
Abstract
Nitric oxide (NO) is a powerful vasodilator in different vascular beds and NO-donors are widely used in clinical practice. Early data suggested that NO and NO-donors activate vascular smooth muscle high-conductance, calcium-activated potassium channels (BK channels). There exist two hypotheses explaining the effect of NO and NO-donors on BK channels-one stating that protein kinase G (PKG) mediates the effect of NO, and the other one stating that NO acts directly on the channel. Thus, the degree of contribution of PKG to the NO-induced activation of the BK channel is still not completely clear. This study tested the hypothesis that the sodium nitroprusside (SNP)-induced activation of vascular smooth muscle BK channels is fully mediated by PKG. This hypothesis was investigated using the patch-clamp technique and freshly isolated smooth muscle cells from rat tail artery. In whole-cell experiments, SNP considerably increased the outward current compared with the addition of the bath solution. SNP did not alter the current in the presence of iberiotoxin, the specific blocker of BK channels, during co-application with hydroxocobalamin, an NO-scavenger, and in the presence of Rp-8-Br-PET-cGMPS, the specific PKG-inhibitor. In inside-out patches, the activity of BK channels was increased by SNP, SNAP, and DEA-NO. However, these effects did not differ from the effect of the application of drug-free bath solution. Furthermore, a similar increase in single BK channel activity was induced by Rp-8-Br-PET-cGMPS, Rp-8-Br-PET-cGMPS together with SNP, hydroxocobalamin, and hydroxocobalamin together with SNP or DEA-NO. Finally, the activity of excised BK channels did not change in the absence of any application but was considerably increased by PKG compared with the addition of drug-free bath solution. These results suggest that NO released from NO-donors stimulates the BK current only through activation of PKG.
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