Nitric Oxide Synthesis from L-Arginine Modulates Renal Vascular Resistance in Isolated Perfused and Intact Rat Kidneys

1991 ◽  
Vol 17 (Supplement) ◽  
pp. 165???168 ◽  
Author(s):  
W. J. Welch ◽  
C. S. Wilcox ◽  
K. Aisaka ◽  
S. S. Gross ◽  
O. W. Griffith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Nitric Oxide Synthesis ◽  
Renal Vascular ◽  
Rat Kidneys

Nitric Oxide Synthesis from l-Arginine Modulates Renal Vascular Resistance in Isolated Perfused and Intact Rat Kidneys

1991 ◽  
Vol 17 (Supplement 3) ◽  
pp. S165-S168 ◽  
Author(s):  
W. J. Welch ◽  
C. S. Wilcox ◽  
K. Aisaka ◽  
S. S. Gross ◽  
O. W. Griffith ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Nitric Oxide Synthesis ◽  
Renal Vascular ◽  
Rat Kidneys

Determinants of renal vasoconstriction after systemic inhibition of nitric oxide synthesis in rats

1996 ◽  
Vol 270 (6) ◽  
pp. R1203-R1207
Author(s):  
E. Brand-Schieber ◽  
M. Pucci ◽  
A. Nasjletti
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Nitric Oxide Synthesis ◽  
Renal Vasoconstriction ◽  
Renal Perfusion Pressure ◽  
Renal Vascular

The effects of NG-nitro-L-arginine (L-NNA, 10 mg/kg i.v.) on renal hemodynamics were examined in control rats, rats in which renal perfusion pressure was prevented from rising after L-NNA by constricting the abdominal aorta, and rats in which tubuloglomerular feedback was inhibited by furosemide pretreatment, ureteral ligation, or both interventions combined. In control rats, L-NNA increased (P < 0.05) renal vascular resistance (274 +/- 27%) along with systemic arterial (54 +/- 4%) and renal perfusion (54 +/- 5%) pressures and decreased (P < 0.05) renal blood flow (57 +/- 4%). In rats in which renal perfusion pressure was prevented from increasing along with systemic arterial pressure (54 +/- 4%), the L-NNA-induced elevation of renal vascular resistance (173 +/- 27%) was less intense (P < 0.05). In another study, where renal perfusion pressure was fixed at pre-L-NNA levels, L-NNA-induced increases in renal vascular resistance (130 +/- 20%) were attenuated (P < 0.05) further with furosemide pretreatment (52 +/- 12%), with ureteral ligation (75 +/- 10%), and with furosemide pretreatment and ureteral ligation combined (32 +/- 8%). These data suggest that vasoconstrictor mechanisms linked to tubuloglomerular feedback and perfusion pressure elevation contribute to renal vasoconstriction after systemic inhibition of nitric oxide synthesis with L-NNA.

scholarly journals Basal and stimulated nitric oxide in control of kidney function in the aging rat

1997 ◽  
Vol 272 (6) ◽  
pp. R1747-R1753 ◽  
Author(s):  
C. Hill ◽  
A. M. Lateef ◽  
K. Engels ◽  
L. Samsell ◽  
C. Baylis
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Renal Vascular Resistance ◽  
Oxidation Products ◽  
No Oxidation ◽  
No Production ◽  
Sprague Dawley ◽  
Vasoconstrictor Response ◽  
Renal Vascular

To investigate the activity of nitric oxide (NO) in control of renal hemodynamics during aging, studies were conducted on conscious Sprague-Dawley rats aged 3-5 mo (young, Y) and 18-22 mo (old, O). Blood pressure (BP) and renal vascular resistance (RVR) were higher in O vs. Y in control, and acute systemic NO synthesis inhibition (NOSI) increased BP and RVR, with an enhanced renal vasoconstrictor response in O. Infusion of the NO substrate L-arginine produced similar, selective renal vasodilation in both groups. The endothelium-dependent vasodilator acetylcholine caused similar falls in BP and RVR, whereas sodium nitroprusside produced an exaggerated depressor response in O vs. Y without falls in RVR in either age group. Urinary excretion of the stable NO oxidation products (NOx) decreased with age, suggesting a decline in the overall somatic NO production. In conclusion, basal tonically produced NO has a more pronounced role in maintenance of renal perfusion in aging, whereas L-arginine- and agonist-stimulated renal vasodilation is not impaired with age. NO production from some source may be reduced with aging, as indicated by falls in 24-h NOX excretion, although the similarity in pressor response and enhanced renal vasoconstrictor response to NOSI suggests that the role of NO in control of total peripheral and renal vascular resistance is maintained.

A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats

2008 ◽  
Vol 294 (6) ◽  
pp. R1847-R1855 ◽  
Author(s):  
Maarten P. Koeners ◽  
Branko Braam ◽  
Dionne M. van der Giezen ◽  
Roel Goldschmeding ◽  
Jaap A. Joles
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Renal Injury ◽  
Renal Vascular Resistance ◽  
Perinatal Exposure ◽  
Hypertensive Rats ◽  
No Donor ◽  
Renal Vascular

Enhancing perinatal nitric oxide (NO) availability persistently reduces blood pressure in spontaneously hypertensive rats. We hypothesize that this approach can be generalized to other models of genetic hypertension, for instance those associated with renal injury. Perinatal exposure to the NO donor molsidomine was studied in fawn-hooded hypertensive (FHH) rats, a model of mild hypertension, impaired preglomerular resistance, and progressive renal injury. Perinatal molsidomine increased urinary NO metabolite excretion at 8 wk of age, i.e., 4 wk after treatment was stopped ( P < 0.05). Systolic blood pressure was persistently reduced after molsidomine (42-wk females: 118 ± 3 vs. 141 ± 5 and 36-wk males: 139 ± 4 vs. 158 ± 4 mmHg; both P < 0.001). Perinatal treatment decreased glomerular filtration rate ( P < 0.05) and renal blood flow ( P < 0.01) and increased renal vascular resistance ( P < 0.05), without affecting filtration fraction, suggesting persistently increased preglomerular resistance. At 4 wk of age natriuresis was transiently increased by molsidomine ( P < 0.05). Molsidomine decreased glomerulosclerosis ( P < 0.05). Renal blood flow correlated positively with glomerulosclerosis in control ( P < 0.001) but not in perinatally treated FHH rats. NO dependency of renal vascular resistance was increased by perinatal molsidomine. Perinatal enhancement of NO availability can ameliorate development of hypertension and renal injury in FHH rats. Paradoxically, glomerular protection by perinatal exposure to the NO donor molsidomine may be due to persistently increased preglomerular resistance. The mechanisms by which increased perinatal NO availability can persistently reprogram kidney function and ameliorate hypertension deserve further study.

Increased Renal Vascular Resistance In Zinc-Deficient Rats: Role Of Nitric Oxide and Superoxide

2002 ◽  
Vol 29 (12) ◽  
pp. 1096-1104 ◽  
Author(s):  
Nobutaka Kurihara ◽  
Hiroyuki Yanagisawa ◽  
Masamichi Sato ◽  
Chang-Kuen Tien ◽  
Osamu Wada
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Vascular

Dose-dependent effects of nitric oxide synthase inhibition on systemic and renal hemodynamics in conscious lambs

1999 ◽  
Vol 77 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Alp Sener ◽  
Francine G Smith
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Vascular Resistance ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Dependent Manner ◽  
Oxide Synthase ◽  
Renal Vascular ◽  
Dose Dependent

The present experiments were carried out to determine the role of nitric oxide in influencing systemic and renal hemodynamics in conscious young sheep. Parameters of cardiovascular function were measured before and for 4 h after intravenous injection of either L-NAME (NG-nitro-L-arginine methyl ester) or D-NAME (NG-nitro-D-arginine methyl ester) at doses of 10, 20, or 40 mg/kg in 13 conscious, chronically instrumented young sheep aged 43 ± 5 days. Blood pressure increased and heart rate decreased in a dose-dependent manner following administration of L-NAME. Renal vascular resistance was increased for 10 min following a dose of 10 mg/kg of L-NAME and for 120 min following a dose of 40 mg/kg of L-NAME. The renal vasodilatory response to close arterial injection of 1 µg/kg of acetylcholine was attenuated by L-NAME in a dose-dependent manner. These experiments provide the first information that under normal physiological conditions in conscious young animals, nitric oxide influences systemic and renal hemodynamics.Key words: renal vascular resistance, renal blood flow, maturation, sheep, vascular tone, nitric oxide, endothelial-derived relaxing factor, L-NAME (NG-nitro-L-arginine methyl ester).

scholarly journals Nitric Oxide/cAMP Interactions in the Control of Rat Renal Vascular Resistance

1999 ◽  
Vol 84 (2) ◽  
pp. 186-192 ◽  
Author(s):  
Peter Sandner ◽  
Mark Kornfeld ◽  
Xiaoping Ruan ◽  
William J. Arendshorst ◽  
Armin Kurtz
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Vascular

Endothelial nitric oxide synthase is predominantly involved in angiotensin II modulation of renal vascular resistance and norepinephrine release

2008 ◽  
Vol 294 (2) ◽  
pp. R421-R428 ◽  
Author(s):  
Johannes Stegbauer ◽  
Yvonne Kuczka ◽  
Oliver Vonend ◽  
Ivo Quack ◽  
Lorenz Sellin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Wild Type ◽  
Norepinephrine Release ◽  
Renal Nerve ◽  
Sympathetic Neurotransmission ◽  
Pressor Responses ◽  
Renal Vascular

Nitric oxide (NO) is mainly generated by endothelial NO synthase (eNOS) or neuronal NOS (nNOS). Recent studies indicate that angiotensin II generates NO release, which modulates renal vascular resistance and sympathetic neurotransmission. Experiments in wild-type [eNOS(+/+) and nNOS(+/+)], eNOS-deficient [eNOS(−/−)], and nNOS-deficient [nNOS(−/−)] mice were performed to determine which NOS isoform is involved. Isolated mice kidneys were perfused with Krebs-Henseleit solution. Endogenous norepinephrine release was measured by HPLC. Angiotensin II dose dependently increased renal vascular resistance in all mice species. EC50 and maximal pressor responses to angiotensin II were greater in eNOS(−/−) than in nNOS(−/−) and smaller in wild-type mice. The nonselective NOS inhibitor Nω-nitro-l-arginine methyl ester (l-NAME; 0.3 mM) enhanced angiotensin II-induced pressor responses in nNOS(−/−) and wild-type mice but not in eNOS(−/−) mice. In nNOS(+/+) mice, 7-nitroindazole monosodium salt (7-NINA; 0.3 mM), a selective nNOS inhibitor, enhanced angiotensin II-induced pressor responses slightly. Angiotensin II-enhanced renal nerve stimulation induced norepinephrine release in all species. l-NAME (0.3 mM) reduced angiotensin II-mediated facilitation of norepinephrine release in nNOS(−/−) and wild-type mice but not in eNOS(−/−) mice. 7-NINA failed to modulate norepinephrine release in nNOS(+/+) mice. (4-Chlorophrnylthio)guanosine-3′, 5′-cyclic monophosphate (0.1 nM) increased norepinephrine release. mRNA expression of eNOS, nNOS, and inducible NOS did not differ between mice strains. In conclusion, angiotensin II-mediated effects on renal vascular resistance and sympathetic neurotransmission are modulated by NO in mice. These effects are mediated by eNOS and nNOS, but NO derived from eNOS dominates. Only NO derived from eNOS seems to modulate angiotensin II-mediated renal norepinephrine release.

scholarly journals L-arginine does not prevent the renal effects of endothelin in humans.

1995 ◽  
Vol 5 (7) ◽  
pp. 1508-1516
Author(s):  
J A Bijlsma ◽  
A J Rabelink ◽  
K A Kaasjager ◽  
H A Koomans
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Renal Vascular Resistance ◽  
Nitric Oxide Production ◽  
Renal Effects ◽  
Renal Vasoconstriction ◽  
Oxide Production ◽  
Renal Vascular ◽  
Stimulation Of

The infusion of endothelin to obtain plasma levels as present in sodium-retaining conditions such as heart failure and hepatorenal syndrome has been shown to cause sodium retention and renal vasoconstriction. Whether these renal effects of endothelin could be modulated by the stimulation of nitric oxide production by the infusion of L-arginine was examined. Therefore, the renal and endocrine effects of the systemic administration of endothelin (2.5 ng/kg per minute for 90 min), L-arginine (5 mg/kg per minute for 90 min), or the combination of endothelin and L-arginine were studied in healthy subjects under clearance conditions. During endothelin infusion, plasma endothelin levels rose from 3.0 +/- 0.2 to 14.1 +/- 2.4 pmol/L (P < 0.01). Mean arterial pressure increased by 7 mm Hg (P < 0.01). The effects on renal function were disproportionately large: renal vascular resistance increased from 77.5 +/- 3.2 to 124.1 +/- 6.7 mm Hg/min per liter (P < 0.01), and sodium excretion fell from 178 +/- 30 to 83 +/- 11 mumol/min (P < 0.01). Endothelin had no effect on urinary nitrite excretion. L-Arginine caused a fall in blood pressure of 5 mm Hg (P < 0.01) and decreased renal vascular resistance by 12% (P < 0.05). Sodium excretion increased twofold. This was associated with an increase in urinary nitrite excretion from 112 +/- 36 to 465 +/- 190 nmol/min (P < 0.01), suggesting stimulation of renal nitric oxide production. During the combination of endothelin and L-arginine, urinary nitrite excretion increased similarly.(ABSTRACT TRUNCATED AT 250 WORDS)

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