Lower than normal expression of brain nitric oxide synthase gene in the hypothalamus of deoxycorticosterone acetate-salt hypertensive rats

Nanbu, Akira; Nishimura, Masato; Takahashi, Hakuo; Ohtsuka, Ken; Sakamoto, Masatoshi; Yoshimura, Manabu

doi:10.1097/00004872-199816040-00011

Cited by 8 publications

(5 citation statements)

References 26 publications

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“…Afferent renal denervation by bilateral dorsal rhizotomy attenuated increases in arterial pressure and urinary excretion of noradrenaline and upregulation of renin, ACE and AT1 receptor mRNAs in the hypothalamus and lower brainstem of subtotally nephrectomized SHR. In our previous studies, expression of nNOS in the hypothalamus was reduced in deoxycorticosterone acetate-salt hypertensive rats, in which expression of the brain AT1 receptor mRNA and peripheral sympathetic nervous activity were upregulated (Nanbu et al 1998, Nishimura et al 1999. Although the precise mechanism is not clear, our results indicate that afferent nerve signals from the remnant kidney are involved in upregulation of renin-angiotensin system mRNAs in the hypothalamus and brainstem as well as hypertension and sympathetic overactivity in this model of chronic renal failure.…”

Section: Discussionsupporting

confidence: 45%

“…Ye et al (2002) have recently reported that losartan, a selective AT1 receptor antagonist, reduced blood pressure and renal sympathetic activity in the phenol renal injury model, and that the effects of losartan were largely mediated by activation of interleukin-1b and neuronal nitric oxide synthase (nNOS) in the posterior hypothalamic nuclei, paraventricular nuclei and locus ceruleus. In our previous studies, expression of nNOS in the hypothalamus was reduced in deoxycorticosterone acetate-salt hypertensive rats, in which expression of the brain AT1 receptor mRNA and peripheral sympathetic nervous activity were upregulated (Nanbu et al 1998, Nishimura et al 1999. Interleukin-1b and particularly nNOS activity in the brain may play a role in connecting the brain reninangiotensin system with sympathetic overactivity in chronic renal failure models.…”

Section: Discussionmentioning

confidence: 87%

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Upregulation of the brain renin–angiotensin system in rats with chronic renal failure

2007

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 87%

Upregulation of the brain renin–angiotensin system in rats with chronic renal failure

2007

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“…This blunted volume reflex resulted in water and sodium retention and overloading in these diseases, which is a major factor in the development and aggravation of these diseases. Furthermore, a decreased NO level or neuronal NOS activity in the hypothalamus or the PVN has been found in heart failure (39,42) and hypertension (11,25). The deficiency of NO in the PVN or other hypothalamic regions may be the major cause of the blunted volume reflex observed in these diseases.…”

Section: Discussionmentioning

confidence: 99%

Role of the paraventricular nucleus in renal excretory responses to acute volume expansion: role of nitric oxide

Mayhan

Patel

2003

American Journal of Physiology-Heart and Circulatory Physiology

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Acute volume expansion (VE) produces a suppression of renal sympathetic nerve discharge (RSND) resulting in diuresis and natriuresis. Recently, we have demonstrated that the endogenous nitric oxide (NO) system within the paraventricular nucleus (PVN) produces a decrease in RSND. We hypothesized that endogenous NO in the PVN is involved in the suppression of RSND leading to diuretic and natriuretic responses to acute VE. To test this hypothesis, we first measured the VE-induced increase in renal sodium excretion and urine flow with and without blockade of NO, with microinjection of NG-monomethyl-L-arginine (L-NMMA; 200 pmol in 200 nl), within the PVN of Inactin-anesthetized male Sprague-Dawley rats. Acute VE produced significant increases in urine flow and sodium excretion, which were diminished in rats treated with L-NMMA within the PVN. This effect of NO blockade within the PVN on VE-induced diuresis and natriuresis was abolished by renal denervation. Consistent with these data, acute VE induced a decrease in RSND (52% of the baseline level), which was significantly blunted by prior administration of L-NMMA into the PVN (28% of the baseline level) induced by a comparable level of acute VE. Using the push-pull perfusion technique, we found that acute VE induced a significant increase in NOx concentration in the perfusate from the PVN region. Taken together, these results suggest that acute VE induces an increase in NO production within the PVN that leads to renal sympathoinhibition, resulting in diuresis and natriuresis. We conclude that NO within the PVN plays an important role in regulation of sodium and water excretions in the volume reflex via modulating renal sympathetic outflow.

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“…Rats with salt-sensitive hypertension have decreased hypothalamic nNOS mRNA expression. 98 It may be postulated that this may limit their ability to reduce sympathetic outflow to the cardiovascular system and the kidney during salt loading. A further site of action of nNOS in the prevention of saltsensitive hypertension may within the kidney itself.…”

Section: Activity Of the Neural No Pathway In Hypertensionmentioning

confidence: 99%

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

Chowdhary

Townend

2001

J Hum Hypertens

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The importance of endothelial nitric oxide (NO) generation in sustaining a tonic systemic vasodilatation is well established. Inhibiting NO production produces hypertension in animals and in humans and not surprisingly there has been considerable interest in establishing whether deficiencies of endothelial NO pathway activity are implicated in the aetiology of essential hypertension. The results of these investigations have been inconsistent with some suggestion that observed deficiencies of both basal and stimulated endothelial NO generation in hypertensive subjects may be an effect rather than the cause of raised arterial pressure. It is increasingly recognised that neuronal production of NO also influences cardiovascular homeostasis through its action as a neuromodulator within the autonomic nervous system. Overall NO has been shown to have sym-

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Lower than normal expression of brain nitric oxide synthase gene in the hypothalamus of deoxycorticosterone acetate-salt hypertensive rats

Cited by 8 publications

References 26 publications

Upregulation of the brain renin–angiotensin system in rats with chronic renal failure

Upregulation of the brain renin–angiotensin system in rats with chronic renal failure

Role of the paraventricular nucleus in renal excretory responses to acute volume expansion: role of nitric oxide

Nitric oxide and hypertension: not just an endothelium derived relaxing factor!

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