ArticleThe Journal of physiology2011
Modulation of the myogenic response in renal blood flow autoregulation by NO depends on endothelial nitric oxide synthase (eNOS), but not neuronal or inducible NOS.
Article in The Journal of physiology, 2011. 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, 27 citations in OpenAlex.
- Angiotensin II augments renal vascular smooth muscle soluble GC expression via an ATBritish journal of pharmacology · 2022Article
- Microvascular dysfunction and kidney disease: Challenges and opportunities?Microcirculation (New York, N.Y. : 1994) · 2021Review
- Impact of the NO-Sensitive Guanylyl Cyclase 1 and 2 on Renal Blood Flow and Systemic Blood Pressure in Mice.International journal of molecular sciences · 2018Article
- Nitric oxide production contributes to Bacillus anthracis edema toxin-associated arterial hypotension and lethality: ex vivo and in vivo studies in the rat.American journal of physiology. Heart and circulatory physiology · 2016Article
- Renal blood flow autoregulation: what are the contributions for nitric oxide or superoxide to modulate the myogenic response?American journal of physiology. Renal physiology · 2016Article
- Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O2- dismutation on renal autoregulation in the time and frequency domains.American journal of physiology. Renal physiology · 2016Article
- Recent advances in research on nitrergic nerve-mediated vasodilatation.Pflugers Archiv : European journal of physiology · 2015Review
- Renal autoregulation in health and disease.Physiological reviews · 2015Review
- Pressure natriuresis and the renal control of arterial blood pressure.The Journal of physiology · 2014Review
- On the selectivity of neuronal NOS inhibitors.British journal of pharmacology · 2013Article
- Renal microvascular dysfunction, hypertension and CKD progression.Current opinion in nephrology and hypertension · 2013Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) blunts the myogenic response (MR) in renal blood flow (RBF) autoregulation. We sought to clarify the roles of NO synthase (NOS) isoforms, i.e. neuronal NOS (nNOS) from macula densa, endothelial NOS (eNOS) from the endothelium, and inducible NOS (iNOS) from smooth muscle or mesangium. RBF autoregulation was studied in rats and knockout (ko) mice in response to a rapid rise in renal artery pressure (RAP). The autoregulatory rise in renal vascular resistance within the first 6 s was interpreted as MR, from ∼6 to ∼30 s as tubuloglomerular feedback (TGF), and ∼30 to ∼100 s as the third regulatory mechanism. In rats, the nNOS inhibitor SMTC did not significantly affect MR (67 ± 4 vs. 57 ± 4 units). Inhibition of all NOS isoforms by l-NAME in the same animals markedly augmented MR to 78 ± 4 units. The same was found when SMTC was combined with angiotensin II to reproduce the hypertension and vasoconstriction seen with l-NAME (58 ± 3 vs. 54 ± 7 units, l-NAME 81 ± 2 units), or when SMTC was replaced by the nNOS inhibitor NPA (57 ± 5 vs. 56 ± 7 units, l-NAME 79 ± 4 units) or by the iNOS inhibitor 1400W (50 ± 1 vs. 55 ± 4 units, l-NAME 81 ± 3 units). nNOS-ko mice showed the same autoregulation as wild-types (MR 36 ± 4 vs. 38 ± 3 units) and the same response to l-NAME (111 ± 9 vs. 114 ± 10 units). eNOS-ko had similar autoregulation as wild-types (44 ± 8 vs. 33 ± 4 units), but failed to respond to l-NAME (37 ± 7 vs. 78 ± 16 units). We conclude that the attenuating effect of NO on MR depends on eNOS, but not on nNOS or iNOS. In eNOS-ko mice MR is depressed by NO-independent means.
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