Relationship between Glomerular Filtration Rate and Tubular Reabsorption of Sodium in Patients with Unilateral Renal Artery Stenosis.

Papanicolaou, N.; Mountokalakis, T.; Safar, M; Milliez, P

doi:10.1159/000180762

Cited by 3 publications

(1 citation statement)

References 22 publications

(24 reference statements)

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“…Note that RBF was calculated from ERPF and could be affected by changes in PAH extraction. Although it is well known that during renal ischemia PAH extraction is reduced, and therefore ERPF grossly underestimated (9,10,29), this does not appear to be the case in essential hypertension (35). Because renal plasma flow was high in control FHH (with the most injury) and fell within the normal range in perinatally treated FHH (Fig.…”

Section: Discussionmentioning

confidence: 96%

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

Koeners¹,

Braam²,

Giezen³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Koeners MP, Braam B, van der Giezen DM, Goldschmeding R, Joles JA. A perinatal nitric oxide donor increases renal vascular resistance and ameliorates hypertension and glomerular injury in adult fawn-hooded hypertensive rats. Am J Physiol Regul Integr Comp Physiol 294: R1847-R1855, 2008. First published April 16, 2008 doi:10.1152/ajpregu.00073.2008.-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 Ͻ 0.05). Systolic blood pressure was persistently reduced after molsidomine (42-wk females: 118 Ϯ 3 vs. 141 Ϯ 5 and 36-wk males: 139 Ϯ 4 vs. 158 Ϯ 4 mmHg; both P Ͻ 0.001). Perinatal treatment decreased glomerular filtration rate (P Ͻ 0.05) and renal blood flow (P Ͻ 0.01) and increased renal vascular resistance (P Ͻ 0.05), without affecting filtration fraction, suggesting persistently increased preglomerular resistance. At 4 wk of age natriuresis was transiently increased by molsidomine (P Ͻ 0.05). Molsidomine decreased glomerulosclerosis (P Ͻ 0.05). Renal blood flow correlated positively with glomerulosclerosis in control (P Ͻ 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. proteinuria; renal hemodynamics; glomerulosclerosis A LARGE BODY OF experimental and epidemiological studies supports the concept that the intrauterine and early postnatal environment interacts with early development in that it can program metabolic and cardiovascular disease (5,18,27). Most of these studies focus on how aberrant perinatal factors increase the occurrence of pathologies in later life. When such factors are superimposed on a specific background of inherited disease, developmental programs will also be affected. Hence, programming can also have long-lasting effects against an abnormal genetic background. Accordingly, advantageous perinatal factors can prevent or correct abnormal development. Because hypertension is associated with decreased nitric oxide (NO) availability (52), it is plausible that factors that support NO availability in the perinatal phase can (re)program development beneficially. This might lead to norm...

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Section: Discussionmentioning

confidence: 96%

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

Koeners¹,

Braam²,

Giezen³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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The performance of renal duplex ultrasonography for the detection of hemodynamically significant renal artery stenosis

Kawarada

Yokoi

Takemoto

et al. 2006

Cathet Cardio Intervent

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Renal effects of the inhibitor of thromboxane A2-synthetase OKY-046

Hatziantoniou

Papanikolaou

1986

Experientia

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Acute renal failure (ARF) was associated with increased urinary thromboxane (TXA2) excretion and lessened excretion of sodium (UNaV) and fractional excretion of sodium (FENa%). The inhibitor of thromboxane A2-synthetase OKY-046 enhanced sodium excretion and fractional excretion of sodium in normal and saline loaded animals whereas it partially prevented the reduction in sodium excretion and creatinine clearance and significantly increased fractional excretion of sodium in glycerol treated rats suggesting a partial protection against the development of acute renal failure.

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Relationship between Glomerular Filtration Rate and Tubular Reabsorption of Sodium in Patients with Unilateral Renal Artery Stenosis.

Cited by 3 publications

References 22 publications

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

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

The performance of renal duplex ultrasonography for the detection of hemodynamically significant renal artery stenosis

Renal effects of the inhibitor of thromboxane A2-synthetase OKY-046

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