scholarly journals Effects of chronic nitric oxide synthase (NOS) inhibition on renal blood flow

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Richard Murray McAllister ◽  
Robert L Johnson ◽  
Sean C Newcomer ◽  
Maurice Harold Laughlin
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Renal Blood Flow ◽  
Oxide Synthase

Nitric oxide synthase and cGMP-mediated stimulation of renin secretion

2001 ◽  
Vol 281 (4) ◽  
pp. R1146-R1151 ◽  
Author(s):  
Cecilia M. Sayago ◽  
William H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Renal Blood Flow ◽  
No Synthase ◽  
Renin Secretion ◽  
Hemodynamic Changes ◽  
Oxide Synthase ◽  
Stimulation Of

The interaction between nitric oxide (NO) and renin is controversial. cAMP is a stimulating messenger for renin, which is degraded by phosphodiesterase (PDE)-3. PDE-3 is inhibited by cGMP, whereas PDE-5 degrades cGMP. We hypothesized that if endogenous cGMP was increased by inhibiting PDE-5, it could inhibit PDE-3, increasing endogenous cAMP, and thereby stimulate renin. We used the selective PDE-5 inhibitor zaprinast at 20 mg/kg body wt ip, which we determined would not change blood pressure (BP) or renal blood flow (RBF). In thiobutabarbital (Inactin)-anesthetized rats, renin secretion rate (RSR) was determined before and 75 min after administration of zaprinast or vehicle. Zaprinast increased cGMP excretion from 12.75 ± 1.57 to 18.67 ± 1.87 pmol/min ( P < 0.003), whereas vehicle had no effect. Zaprinast increased RSR sixfold (from 2.95 ± 1.74 to 17.62 ± 5.46 ng ANG I · h−1 · min−1, P< 0.024), while vehicle had no effect (from 4.08 ± 2.02 to 3.87 ± 1.53 ng ANG I · h−1 · min−1). There were no changes in BP or RBF. We then tested whether the increase in cGMP could be partially due to the activity of the neuronal isoform of NO synthase (nNOS). Pretreatment with the nNOS inhibitor 7-nitroindazole (7-NI; 50 mg/kg body wt) did not change BP or RBF but attenuated the renin-stimulating effect of zaprinast by 40% compared with vehicle. In 7-NI-treated animals, zaprinast-stimulated cGMP excretion was attenuated by 48%, from 9.17 ± 1.85 to 13.60 ± 2.15 pmol/min, compared with an increase from 10.94 ± 1.90 to 26.38 ± 3.61 pmol/min with zaprinast without 7-NI ( P < 0.04). This suggests that changes in endogenous cGMP production at levels not associated with renal hemodynamic changes are involved in a renin-stimulatory pathway. One source of this cGMP may be nNOS generation of NO in the kidney.

scholarly journals Temporal patterns of blood flow and nitric oxide synthase expression affect macrophage accumulation and proliferation during collateral growth

2010 ◽  
Vol 2 (1) ◽  
pp. 18 ◽  
Author(s):  
Hendrik B Sager ◽  
Ralf Middendorff ◽  
Kim Rauche ◽  
Joachim Weil ◽  
Wolfgang Lieb ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Temporal Patterns ◽  
Collateral Growth ◽  
Oxide Synthase ◽  
Macrophage Accumulation

Nitric oxide synthase inhibition in healthy adults reduces regional and total cerebral macrovascular blood flow and microvascular perfusion

2021 ◽  
Author(s):  
Katrina J. Carter ◽  
Aaron T. Ward ◽  
J. Mikhail Kellawan ◽  
Marlowe W. Eldridge ◽  
Awni Al‐Subu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Healthy Adults ◽  
Microvascular Perfusion ◽  
Oxide Synthase

scholarly journals Rapid nontranscriptional activation of endothelial nitric oxide synthase mediates increased cerebral blood flow and stroke protection by corticosteroids

2003 ◽  
Vol 111 (5) ◽  
pp. 759-759
Author(s):  
Florian P. Limbourg ◽  
Zhihong Huang ◽  
Jean-Christophe Plumier ◽  
Tommaso Simoncini ◽  
Masayuki Fujioka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide
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