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.

Hypoxia inhibits nitric oxide synthesis in isolated rabbit lung

1997 ◽  
Vol 272 (6) ◽  
pp. L1167-L1173 ◽  
Author(s):  
S. P. Kantrow ◽  
Y. C. Huang ◽  
A. R. Whorton ◽  
E. N. Grayck ◽  
J. M. Knight ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Competitive Inhibitor ◽  
Oxidation Products ◽  
No Oxidation ◽  
Severe Hypoxia ◽  
No Production ◽  
Rabbit Lung ◽  
Vasoconstrictor Response ◽  
Hypoxic Vasoconstriction ◽  
Oxide Synthase

Nitric oxide (NO.) has been proposed to modulate hypoxic vasoconstriction in the lung. The activity of nitric oxide synthase (NOS) can be inhibited by hypoxia because molecular oxygen is a necessary substrate for the enzyme. On the basis of this mechanism, we hypothesized that NOS activity has a key role in regulation of pulmonary vascular tone during hypoxia. We measured oxidation products of NO. released into the vasculature of isolated buffer-perfused rabbit lung ventilated with normoxic (21% O2), moderately hypoxic (5% O2), or anoxic (0% O2) gas using two methods. Mean PO2 in perfusate exiting the lung was 25 Torr during anoxic ventilation and 47 Torr during moderately hypoxic ventilation. We found that the amount of the NO. oxidation product nitrite released into the perfusate was suppressed significantly during ventilation with anoxic but not moderately hypoxic gas. During normoxic ventilation, nitrite release was inhibited by pretreatment with NG-monomethyl-L-arginine, a competitive inhibitor of NOS. To confirm that changes in nitrite concentration reflected changes in NO. release into the perfusate, major oxidation products of NO. (NOx) were assayed using a method for reduction of these products to NO. by vanadium(III) Cl. Release of NOx into the perfusate was suppressed by severe hypoxia (anoxic ventilation), and this effect was reversed by normoxia. Pulmonary vasoconstriction was observed during severe but not moderate hypoxia and was related inversely to the rate of nitrite release. These observations provide evidence that decreased NO. production contributes to the pulmonary vasoconstrictor response during severe hypoxia.

Sexual dimorphism in regional blood flow responses to vasopressin in conscious rats

1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Regional Blood Flow ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Female Rats ◽  
Sexually Dimorphic ◽  
Arterial Blood ◽  
Vasoconstrictor Response ◽  
Renal Vascular

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.

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

Role of erythropoietin and nitric oxide in modulating the tone of human renal interlobular and subcutaneous arteries from uraemic subjects

1999 ◽  
Vol 97 (6) ◽  
pp. 639-647 ◽  
Author(s):  
Xiao Chun WU ◽  
Nicholas T. RICHARDS ◽  
Edward J. JOHNS
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Methyl Ester ◽  
Vascular Resistance ◽  
No Production ◽  
Resting Tension ◽  
Acute Responses ◽  
Resting Tone ◽  
Renal Vascular

This study investigated potential reasons why erythropoietin (EPO) given therapeutically to patients with renal failure may increase peripheral, but not renal, vascular resistance. This was done by comparing the effects of EPO on resting tension in normal renal interlobular and subcutaneous vessels from uraemic patients. In human subcutaneous arteries from uraemic subjects, noradrenaline- and KCl-induced vasoconstrictions were enhanced when nitric oxide (NO) production was blocked with NG-nitro-L-arginine methyl ester (L-NAME), but were unaffected by EPO, while acetylcholine- and bradykinin-induced concentration-dependent relaxations were markedly attenuated by L-NAME, but not by EPO. The noradrenaline- and KCl-induced vasoconstrictions of human renal interlobular arteries were unaffected by the presence of L-NAME, but were attenuated by EPO (20 units·ml-1) by some 33% (P< 0.01); this effect was enhanced by the co-administration of L-NAME. Acetylcholine and bradykinin caused comparable dilatations of the interlobular arteries; the response to the former was attenuated by L-NAME, but none of these responses were changed by EPO. EPO given alone, at a concentration of either 0.1 or 20 units·ml-1, had no effect on basal resting tone. NO production mediated both acetylcholine- and bradykinin-induced relaxation in this vessel type. In contrast, in the interlobular arteries there was no indication of NO modulating the level of vasoconstriction, and it only mediated acetylcholine-induced dilation. These acute responses to EPO only partially explain its differential effects on the vasculature in renal failure.

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

A renal vasodilator effect of angiotensin II revealed by dual thromboxane inhibition

1994 ◽  
Vol 72 (6) ◽  
pp. 632-636 ◽  
Author(s):  
Al-Hassan Badahman ◽  
Thomas W. Wilson
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Sprague Dawley ◽  
Synthesis Inhibition ◽  
Renal Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Renal Vascular ◽  
Arachidonate Release ◽  
Stimulation Of

Angiotensin II (AII) stimulates arachidonate release from renal endothelial and other ceils. Arachidonate is then metabolized by cyclooxygenase to prostaglandin (PG) H2, then PGI2 and thromboxane A2 (TXA2). PGH2 and TXA2 activate the same receptor and should augment AII-mediated vasoconstriction, whereas PGI2 is a vasodilator. We had previously shown that inhibiting TXA2 synthesis with furegrelate (FRG) redirects PGH2 metabolism toward PGI2, causing renal vasodilation. Because TXA2 synthesis inhibition may be incomplete and unmetabolized PGH2 may cause vasoconstriction, we reasoned that adding a PGH2/TXA2 receptor antagonist (BMS 180,290, formerly SQ 29548 (SQ)) to furegrelate should cause further renal vasodilation in the presence of AII Eight groups of 10 Sprague–Dawley rats received 120-min intravenous infusions of vehicle, FRG (2 mg∙kg−1 plus 2 mg∙kg−1∙h−1), SQ (2 mg∙kg−1 plus 2 mg∙kg−1∙h−1), FRG plus SQ, AII (10 ng∙kg−1∙min−1), AII plus FRG, AII plus SQ, or AII plus FRG plus SQ. Mean arterial pressure (MAP), p-[14C]aminohippurate clearance (CPAH), and [3H]insulin clearance were averaged for each rat for the final 90 min in three clearance periods. MAP did not change with any treatment. Estimating renal vascular resistance as MAP/CPAH confirmed a renal vasoconstrictor effect of this dose of AII: 58.1 ± 6.3 vs. 47.3 ± 6.8 (arbitrary units) with the vehicle (p < 0.05). FRG, SQ, or their combination did not affect renal vascular resistance, but adding FRG or SQ to AII prevented AII-mediated renal vasoconstriction. Adding both to AII caused net renal vasodilation to 24.8 ± 2.6 (p < 0.05 vs. vehicle). Inulin clearance changed in the same direction in all groups, but the changes were less marked. We conclude that stimulation of renal arachidonate release by AII combined with TXA2 synthesis inhibition and receptor antagonism results in vasodilation. This renal effect could be due to increased and unopposed renal vasodilator PG (principally PGI2) action.Key words: renal hemodynamics, angiotensin II, prostaglandins, thromboxane.

Myogenic contribution to agonist-induced renal vasoconstriction during normoxia and hypoxia

1997 ◽  
Vol 272 (4) ◽  
pp. H1945-H1951 ◽  
Author(s):  
M. R. Eichinger ◽  
J. M. Resta ◽  
B. R. Walker
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Acute Hypoxia ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Renal Vascular

Acute hypoxia attenuates agonist-induced constrictor and pressor responses in conscious rats, and a recent report suggests that hypoxia may also diminish myogenic reactivity in isolated, perfused rat kidneys. Thus we hypothesized that the diminished responsiveness to pressor agents during hypoxia is caused by an impairment of myogenic reactivity. Male Sprague-Dawley rats were instrumented with a pulsed Doppler flow probe on the left renal artery, an aortic vascular occluder cuff immediately above the left renal artery to control renal perfusion pressure, and catheters were inserted to measure systemic arterial blood pressure and renal arterial pressure (RAP) and for administration of agents. Animals were studied under normoxic or acute hypoxic (fractional concentration of O2 in inspired gials = 0.12) conditions and were administered phenylephrine, arginine vasopressin, or angiotensin II. To determine the myogenic (pressure-dependent) component of agonist-induced vasoconstriction, renal vascular resistance was calculated during agonist infusion with RAP uncontrolled and with RAP controlled to preinfusion levels. Significant myogenic components of agonist-induced renal vasoconstriction were evident with all pressor agents used. However, hypoxia did not attenuate agonist-induced, pressure-dependent increases in renal vascular resistance. We conclude that the reduced vasoreactivity associated with acute hypoxia is not caused by diminished myogenic reactivity.

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
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