Blockade of nitric oxide formation inhibits the stimulation of the renin system by a low salt intake

Schricker, K. Th.; Kurtz, Armin

doi:10.1007/s004240050123

Cited by 20 publications

(20 citation statements)

References 24 publications

(47 reference statements)

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“…Figure 1 shows that l-NAME-treated rats had a significantly higher control period MAP, averaging 124 ± 1 mmHg in the HSL rats and 116 ± 1 mmHg in the LSL group. Although the difference was mild, this evidence of salt-sensitivity during chronic l-NAME infusion is consistent with previous reports [22][23][24][25] and also is supported by the blunted effect of salt intake to change PRA in the l-NAME rats; for example, an approximate threefold difference in PRA between high and low salt compared with the eightfold difference between the vehicle rats during the control period.…”

Section: Resultssupporting

confidence: 89%

Lack of Blood Pressure Salt‐sensitivity Supports a Preglomerular Site of Action of Nitric Oxide in Type I Diabetic Rats

Brands

Bell

Fleming

et al. 2007

Clin Exp Pharma Physio

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1. The relationship between sodium intake and blood pressure is affected differently by changes in angiotensin (Ang) II and preglomerular resistance, and this study measured that relationship to evaluate the link between nitric oxide and blood pressure early in diabetes. 2. Rats were chronically instrumented, placed on high-sodium (HS = 12 mEq/d) or low-sodium (LS = 0.07 mEq/d) intake diets and assigned to either vehicle- (V) or Nomega-nitro-L-arginine methyl ester- (L-NAME; L) treated groups. Mean arterial pressure (MAP) was measured 18 h/day for a 6-day control and 14-day streptozotocin diabetic period in each animal. 3. The MAP of the control period averaged 95 +/- 1 and 94 +/- 1 mmHg in the LSV and HSV rats and 116 +/- 2 and 124 +/- 1 mmHg in the LSL and HSL rats, respectively (LSL vs HSL was significant at P < 0.05). Diabetes increased MAP only in the LSL and HSL rats to 141 +/- 2 mmHg and 152 +/- 2, respectively, similar to our previous reports, and those respective 25 and 28 mmHg increases were a parallel shift in the pressure natriuresis relationship. However, the apparent difference between the LSL and HSL groups when compared was a parallel of the control MAP difference. Plasma renin activity (PRA) in the control period averaged 1.5 +/- 0.5 and 8.1 +/- 1.8 ng AI/mL per h in the HSV and LSV rats, and 0.8 +/- 0.2 and 2.8 +/- 0.5 ng AI/mL per h in the HSL and LSL rats, respectively, and increased similarly by 4.6-fold in the HSL and 4.8-fold in the LSL rats during diabetes. Glomerular filtration rate (GFR) increased in the vehicle but not the L-NAME-treated groups, consistent with our previous reports. 4. Thus, the hypertension caused by the onset of diabetes in L-NAME-treated rats was not salt-sensitive. The normal modulation of PRA by salt intake and the failure of GFR to increase are consistent with our hypothesis that nitric oxide may protect against hypertension early in diabetes by preventing preglomerular vasoconstriction by AngII.

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Section: Resultssupporting

confidence: 89%

Lack of Blood Pressure Salt‐sensitivity Supports a Preglomerular Site of Action of Nitric Oxide in Type I Diabetic Rats

Brands

Bell

Fleming

et al. 2007

Clin Exp Pharma Physio

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“…This suppression of renin release is independent of the associated increase in renal perfusion pressure, sodium chloride excretion [95] and reflex neuronal activity [111]. Furthermore NO inhibition attenuates the renin response to a low-salt diet [109] and pressure-dependent renin release [112], suggesting a necessity for NO to be present for the normal renin response to salt depletion and low blood pressure. In studies using cultured juxta glomerular cells, NO appears to stimulate renin release [113][114][115] and this is dependent on extracellular Ca 2+ [116].…”

Section: No and Reninmentioning

confidence: 95%

“…Most in vivo studies demonstrate a reduced renin concentration in association with NO inhibition [21, 23, 25, 95, 106-108], including a concomitant reduction in kidney renin mRNA expression [109], even though NO is known to preferentially dilate the afferent arteriole of the renal glomerulus [110]. This suppression of renin release is independent of the associated increase in renal perfusion pressure, sodium chloride excretion [95] and reflex neuronal activity [111].…”

Section: No and Reninmentioning

confidence: 98%

Vascular endothelium and nitric oxide in childhood hypertension

Goonasekera

Dillon

1998

Pediatric Nephrology

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Vascular endothelium releases nitric oxide (NO), an important vasodilator that is continuously synthesised by the constitutive enzyme, endothelial nitric oxide synthase (NOS). This maintains a constant vasodilator tone which is diminished in adult hypertension, due to reduced endothelium-dependent vascular relaxation, which is NO dependent. In childhood, however, hypertension is often secondary, and normalisation of blood pressure by removal of cause (e.g. renal artery stenosis, catecholamine-producing tumour) suggests reversibility of endothelial dysfunction, if it is present. Raised plasma levels of endogenous inhibitors have been found, especially in children with secondary hypertension due to renal parenchymal and renovascular disease, and may contribute to hypertension by more than just inhibition of vascular NO release; e.g. by reduction of glomerular filtration rate and promotion of salt and water retention. These inhibitors also modulate renin release, which may be of relevance in cardiovascular physiology, and may also interfere with the anti-platelet properties of NO, increasing the likelihood of vascular thrombotic events. NO inhibitors also promote endothelial activation, with increased expression of adhesion molecules that may form seedlings of atherosclerosis. In chronic renal impairment, accumulation of NO inhibitors may contribute to hypertension. Efficient long-session dialysis helps better interdialysis control of blood pressure in these subjects, independent of salt and water removal, suggesting that removal of such vasoactive agents may be important for efficient blood pressure control. There are a few studies assessing NO generation in hypertensive children via plasma nitrite and nitrate, the NO end products, which suggest normal or increased production as opposed to a reduction, perhaps as a compensatory phenomenon. In the treatment of hypertension, nitroprusside and nitrates exert their actions via NO donation. Excessive production of NO (usually via inducible NOS) or excessive administration (nitrovasodilators) can be cytotoxic and may cause hypotension and shock, as in severe sepsis. NOS inhibitors and NO therefore appear to play a crucial role in aetiology, complications and therapy of childhood hypertension.

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“…Thus, Fujihara et al (1994) found that chronic administration of the non-specific NOS inhibitor L-NAME blocks the inhibitory effect of a high sodium diet on PRA, and Schricker & Kurtz (1996) observed that the non-specific blockade of nitric oxide formation inhibits the stimulation of the renin system by a low salt intake. These results are also in line with the finding by Beierwaltes (1997) that chronic nNOS blockade reverses the effect of low salt intake on renin release.…”

Section: Figurementioning

confidence: 99%

Chronic Blockade of Neuronal Nitric Oxide Synthase Does Not Affect Long‐Term Control of Blood Pressure in Normal, Saline‐Drinking or Deoxycorticosterone‐Treated Rats

Wangensteen

Sainz

Rodríguez-Gómez

et al. 2003

Experimental Physiology

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It has been reported that long‐term selective inhibition of neuronal nitric oxide synthase (nNOS) produces elevated blood pressure (BP) in normal rats. The present study was designed to analyse the possible influences of the sodium‐retaining hormone deoxycorticosterone acetate (DOCA) and of an increased sodium intake on BP effects induced by the chronic blockade of nNOS with 7‐nitroindazole (7NI). Two experiments were performed using 7NI at a dose of either 10 mg kg−1 day−1 (experiment 1) or 30 mg kg−1 day−1 (experiment 2). The following groups were used in both experiments: control rats, and rats that received either 1% saline drinking water (Salt), deoxycorticosterone acetate (DOCA), 7NI, 7NI plus 1% saline (7NI + Salt) or 7NI plus DOCA (7NI + DOCA). The tail systolic BP (SBP) was measured in all rats once a week. At the end of the experimental period, the mean arterial pressure (MAP) and metabolic, morphological and renal variables were measured. There were no significant differences in the tail SBP, final MAP or glomerular filtration rate between the experimental groups and the control group. In both experiments, the plasma renin activity (PRA) was significantly inhibited in the Salt groups and suppressed in the DOCA groups. The PRA significantly increased in the 7NI groups, whereas the 7NI + Salt and 7NI + DOCA groups showed a significant inhibition in PRA, especially compared to the 7NI groups in the two experiments. We conclude that chronic nNOS blockade is unable to increase BP in normal, saline‐drinking or DOCA‐treated rats. Furthermore, the nNOS blockade does not interfere with the counterbalance between renin and an increased sodium intake or retention.

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Blockade of nitric oxide formation inhibits the stimulation of the renin system by a low salt intake

Cited by 20 publications

References 24 publications

Lack of Blood Pressure Salt‐sensitivity Supports a Preglomerular Site of Action of Nitric Oxide in Type I Diabetic Rats

Lack of Blood Pressure Salt‐sensitivity Supports a Preglomerular Site of Action of Nitric Oxide in Type I Diabetic Rats

Vascular endothelium and nitric oxide in childhood hypertension

Chronic Blockade of Neuronal Nitric Oxide Synthase Does Not Affect Long‐Term Control of Blood Pressure in Normal, Saline‐Drinking or Deoxycorticosterone‐Treated Rats

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