Role of nitric oxide on the central hemodynamic response to acute volume expansion in the pregnant rat

Pregnancy is characterized by plasma volume expansion and renal sodium retention with loss of natriuretic response to atrial natriuretic peptide due to increased medullary phosphodiesterase-5 (PDE5). Here, we determined whether natriuretic responses to nitric oxide (NO) are also blunted in pregnancy due to increased PDE5. Anesthetized 16-day pregnant and virgin rats were studied at baseline and during intrarenal infusion of the NO donor spermine NONOate (2.5 nmol/min), the PDE5 inhibitor sildenafil (SILD; 0.5 μg/min), or a combination. The right (noninfused) kidney served as a control. Intrarenal NONOate had no effect on mean arterial pressure (MAP); however, SILD reduced MAP in virgin rats, and the combination of NONOate+SILD reduced MAP in both virgin and pregnant rats. Neither NONOate nor SILD altered glomerular filtration rate. NONOate and SILD each stimulated sodium excretion (UNaV) and fractional excretion of sodium (FENa) in virgin rats, but the combination did not result in an additional natriuretic response. However, NONOate infusion did not increase UNaV or FENa in pregnant rats, but the natriuretic response to NONOate was restored with SILD, and SILD alone produced a natriuresis during pregnancy. Sodium nitroprusside (10−4 mol/l)-stimulated cGMP accumulation from inner medullary collecting duct cells was blunted in cells from pregnant vs. virgin or postpartum rats and was restored by treatment with the PDE5 inhibitor DMPPO (10−7 mol/l). Therefore, increased intrarenal PDE5 mediates the blunted natriuretic response to NO, and loss of responsiveness to the cGMP-dependent, natriuretic agents may contribute to volume expansion during pregnancy.

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Role of nitric oxide in mediating renal response to volume expansion.

Hypertension ◽

10.1161/01.hyp.19.6.780 ◽

1992 ◽

Vol 19 (6_pt_2) ◽

pp. 780-784 ◽

Cited By ~ 61

Author(s):

A Alberola ◽

J M Pinilla ◽

T Quesada ◽

J C Romero ◽

M G Salom ◽

...

Keyword(s):

Nitric Oxide ◽

Volume Expansion ◽

Renal Response

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Role of nitric oxide in the renal hemodynamic response to a meat meal

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1994.267.4.r1050 ◽

1994 ◽

Vol 267 (4) ◽

pp. R1050-R1055 ◽

Cited By ~ 6

Author(s):

F. J. Salazar ◽

A. Alberola ◽

T. Nakamura ◽

J. P. Granger

Keyword(s):

Nitric Oxide ◽

Filtration Rate ◽

Renal Plasma Flow ◽

Hemodynamic Response ◽

Synthesis Inhibition ◽

Renal Hemodynamic ◽

Meat Meal ◽

Induced Changes ◽

Chronically Instrumented Dogs

Ingestion of a high-protein meat meal results in significant increases in renal plasma flow (RPF) and glomerular filtration rate (GFR). The mechanism involved in this hemodynamic response to the meat meal has not yet been fully elucidated. The present study was designed to test the hypothesis that nitric oxide (NO) is involved in the renal hyperemic responses to a meat meal. To test this hypothesis, renal hemodynamic response to a meat meal (10 g/kg) was determined in conscious, chronically instrumented dogs with (n = 9) and without (n = 7) an intrarenal NO synthesis inhibition with NG-nitro-L-arginine methyl ester (L-NAME, 3 micrograms.kg-1.min-1 intrarenally). Under control conditions, the meat meal resulted in significant renal hyperemia. Three hours after ingestion of the meat meal, GFR (43 +/- 3 to 59 +/- 6 ml/min) and RPF (128 +/- 10 to 160 +/- 17 ml/min) progressively increased by approximately 40 and 25%, respectively. In contrast, pretreatment with intrarenal infusion of L-NAME abolished the GFR (48 +/- 6 to 52 +/- 6 ml/min) and RPF (129 +/- 20 to 121 +/- 17 ml/min) increases induced by the meat meal. Pretreatment with L-arginine (0.5 mg.kg-1.min-1) plus L-NAME (3 micrograms.kg-1.min-1) did not modify the meat meal-induced changes in GFR (41 +/- 4 to 66 +/- 6 ml/min) and RPF (127 +/- 9 to 182 +/- 14 ml/min). In summary, a meat meal in dogs results in marked increases in RPF and GFR. Intrarenal NO synthesis inhibition abolished the RPF and GFR responses to the meat meal.(ABSTRACT TRUNCATED AT 250 WORDS)

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Role of nitric oxide in modulating renal function and arterial pressure during chronic aldosterone excess

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1999.276.1.r197 ◽

1999 ◽

Vol 276 (1) ◽

pp. R197-R202 ◽

Cited By ~ 3

Author(s):

Joey P. Granger ◽

Salah Kassab ◽

Jacqueline Novak ◽

Jane F. Reckelhoff ◽

Brett Tucker ◽

...

Keyword(s):

Nitric Oxide ◽

Arterial Pressure ◽

Volume Expansion ◽

Renal Plasma Flow ◽

Extracellular Fluid ◽

Sodium Retention ◽

Long Term Effects ◽

Synthesis Inhibitor

Chronic aldosterone (Aldo) excess is associated with transient sodium retention, extracellular fluid volume expansion, renal vasodilation, and hypertension. The purpose of this study was to determine the role of nitric oxide (NO) in mediating the renal vasodilation and the escape from the sodium-retaining actions of Aldo. To achieve this goal, we examined the long-term effects of Aldo (15 μg ⋅ kg−1 ⋅ min−1for 7 days) in conscious, chronically instrumented control dogs ( n = 9) and in dogs ( n = 12) pretreated with the NO synthesis inhibitor N G-nitro-l-arginine methyl ester (l-NAME; 10 μg ⋅ kg−1 ⋅ min−1). In control dogs, Aldo caused a transient sodium retention (126 ± 6 to 56 ± 2 meq/day) followed by a return of sodium excretion to normal levels. Aldo also increased renal plasma flow by 15% (205 ± 13 to 233 ± 16 ml/min), glomerular filtration rate by 20% (72 ± 3 to 87 ± 5 ml/min), and arterial pressure from 90 ± 3 to 102 ± 3 mmHg. Aldo increased urinary nitrate/nitrite excretion by 60% in the control dogs. Although the sodium-retaining (144 ± 7 to 56 ± 7 meq/day) and arterial pressure (122 ± 6 to 136 ± 5 mmHg) responses to Aldo were the same in dogs pretreated withl-NAME compared with control, the renal hemodynamic response was markedly attenuated. The results of this study suggest that NO plays an important role in mediating the renal vasodilation during chronic Aldo excess.

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Modulated hemodynamic response to clonidine in bile duct-ligated rats: The role of nitric oxide

European Journal of Pharmacology ◽

10.1016/j.ejphar.2006.04.052 ◽

2006 ◽

Vol 542 (1-3) ◽

pp. 148-153 ◽

Cited By ~ 6

Author(s):

Sina Tavakoli ◽

Amir Reza Hajrasouliha ◽

Pejman Jabehdar-Maralani ◽

Farzad Ebrahimi ◽

Hamed Sadeghipour ◽

...

Keyword(s):

Nitric Oxide ◽

Bile Duct ◽

Hemodynamic Response

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Effect of an Inhibitor of Neuronal Nitric Oxide Synthase 7-Nitroindazole on Cerebral Hemodynamic Response and Brain Excitability in Urethane-Anesthetized Rats

Physiological Research ◽

10.33549/physiolres.932564 ◽

2013 ◽

pp. S57-S66 ◽

Cited By ~ 5

Author(s):

C. BROŽÍČKOVÁ ◽

J. OTÁHAL

Keyword(s):

Nitric Oxide ◽

Blood Pressure ◽

Nitric Oxide Synthase ◽

Neurovascular Coupling ◽

Neuronal Nitric Oxide Synthase ◽

Hemodynamic Response ◽

Doppler Flowmetry ◽

Arterial Blood ◽

Oxide Synthase

The role of neuronal nitric oxide synthase (nNOS) in the pathophysiology of epilepsy and seizures remains disputable. One of the reasons why results from the acute in vivo studies display controversies might be the effect on the regulation of cerebral blood flow (CBF) during pharmacologically induced alterations of NO system. We examined neurovascular coupling in the rat sensorimotor cortex in response to transcallosal stimulation under nNOS inhibition by 7-nitroindazole (7-NI). Adult Wistar rats were anesthetized with urethane and epidural silver EEG electrodes were implanted over sensorimotor cortices. Regional CBF was measured by Laser Doppler Flowmetry (LDF). We catheterized a common carotid artery to measure arterial blood pressure (BP). 7-NI did not significantly affect blood pressure and heart rate. Electrophysiological recordings of evoked potentials (EPs) revealed no effect on their amplitude, rhythmic potentiation or depression of EPs. Transcallosal stimulation of the contralateral cortex induced a frequency dependent rise in CBF. Although 7-NI did not significantly affect basal CBF and cortical excitability, hemodynamic responses to the transcallosal stimulation were diminished implicating a role of nNOS in neurovascular coupling. Urethane anesthesia is suitable for future epileptological experiments. Our findings demonstrate that NO contributes to the hemodynamic response during brain activation.

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