Nitric oxide (NO) modulates the neurogenic control of blood pressure in rats with chronic renal failure (CRF).

Ye, S; Nosrati, Saeid; Campese, Vito M.

doi:10.1172/jci119191

Cited by 95 publications

(66 citation statements)

References 56 publications

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“…A substantial body of work has shown that central or peripheral blockade of NO synthesis potentiates or prolongs the pressor response to ANG II (9,28,31,33), upregulates AT 1 expression, and activates cardiovascular angiotensin-converting enzyme (49). On the other hand, ANG II has been found to regulate NOS activity and NO release (27,57). Li et al (28) reported that push-pull administration of ANG II into the PVN induced an increase in NO release.…”

Section: Discussionmentioning

confidence: 99%

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

Xue¹,

Singh²,

Guo³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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.-The present study tested the hypotheses that 1) nitric oxide (NO) is involved in attenuated responses to ANG II in female mice, and 2) there is differential expression of neuronal NO synthase (nNOS) in the subfornical organ (SFO) and paraventricular nucleus (PVN) in response to systemic infusions of ANG II in males vs. females. Aortic blood pressure (BP) was measured in conscious mice with telemetry im-), an inhibitor of NOS, was administrated into the lateral cerebral ventricle for 14 days before and during ANG II pump implantation. Central infusion of L-NAME augmented the pressor effects of systemic ANG II in females (⌬21.5 Ϯ 2.2 vs. ⌬9.2 Ϯ 1.5 mmHg) but not in males (⌬29.4 Ϯ 2.5 vs. ⌬30.1 Ϯ 2.5 mmHg). Central administration of, a selective nNOS inhibitor, also significantly potentiated the increase in BP induced by ANG II in females (⌬17.5 Ϯ 3.2 vs. ⌬9.2 Ϯ 1.5 mmHg). In gonadectomized mice, central L-NAME infusion did not affect the pressor response to ANG II in either males or females. Ganglionic blockade after ANG II infusion resulted in a greater reduction in BP in central L-NAME-or L-VNIO-treated females compared with control females. Western blot analysis of nNOS protein expression indicated that levels were ϳ12-fold higher in both the SFO and PVN of intact females compared with those in intact males. Seven days of ANG II treatment resulted in a further increase in nNOS protein expression only in intact females (PVN, to ϳ51-fold). Immunohistochemical studies revealed colocalization of nNOS and estrogen receptors in the SFO and PVN. These results suggest that NO attenuates the increase in BP induced by ANG II through reduced sympathetic outflow in females and that increased nNOS protein expression associated with the presence of female sex hormones plays a protective role against ANG II-induced hypertension in female mice. sex hormone; nitric oxide/nitric oxide synthase; blood pressure NITRIC OXIDE (NO) and angiotensin II (ANG II) are important agents that regulate arterial blood pressure (BP). Vasoconstriction produced by sympathoexcitatory effects contributes to ANG II-induced pressor responses (13, 17). Conversely, NO has a hypotensive action via vasodilation and sympathoinhibition (36, 39). It has been shown that interactions between ANG II and NO occur in a variety of tissues, including the central nervous system (CNS) (40, 58). For example, microinjection of either an NO synthase (NOS) inhibitor or ANG II into the lateral ventricle or the paraventricular nucleus (PVN) increases the discharge of renal sympathetic nerves and elevates arterial BP and heart rate (HR) (25, 28, 52). Central or peripheral blockade of NOS potentiates or prolongs the pressor response to ANG II (9, 31). Conversely, overexpression of neuronal NOS (nNOS) within the PVN by adenoviral gene transfer significantly attenuates ANG II pressor responses (28).There is evidence from human and animal studies that hypertension is delayed and attenuated in females compared with males (11). Previous studies from our laboratory (54) have sh...

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Section: Discussionmentioning

confidence: 99%

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

Xue¹,

Singh²,

Guo³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…In this model of neurogenic hypertension, the increase in BP is caused by injecting 50 l of 10% phenol into the lower pole of one kidney. 33 Injection of phenol leads to an immediate rise in BP, norepinephrine secretion from the posterior hypothalamus, and renal sympathetic nerve activation, which again can be prevented by renal denervation. 33 Of note, these effects are long lasting and do not occur with infusion of vehicle.…”

Section: Renal Injury and Ischemiamentioning

confidence: 99%

“…33 Injection of phenol leads to an immediate rise in BP, norepinephrine secretion from the posterior hypothalamus, and renal sympathetic nerve activation, which again can be prevented by renal denervation. 33 Of note, these effects are long lasting and do not occur with infusion of vehicle. 34 In conjunction with the demonstration of elevated sympathetic activity in experimental renal artery stenosis 35 Figure 1.…”

Section: Renal Injury and Ischemiamentioning

confidence: 99%

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Sympathetic Activation in Chronic Renal Failure

Schlaich

Socratous

Hennebry

et al. 2009

Journal of the American Society of Nephrology

371

237

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“…However, the mechanism for autonomic regulation of arterial pressure in responses to a dramatic rise in circulating catecholamines during transition is not known. Recent studies (34) have reported that the NE turnover rate in brain nuclei is associated with nNOS mRNA expression and NO content in chronic renal failure rats. In adult rats, coexistence of NADPHd/nNOS and TH in brain nuclei has been demonstrated and suggests that noradrenergic neurons are capable of generating NO for regulation of noradrenergic activity within the brain (25,31).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular regulation and expressions of NO synthase-tyrosine hydroxylase in nucleus tractus solitarius of ovine fetus

Fang

Morgan

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Ma, Sheng-Xing, Qun Fang, Brian Morgan, Michael G. Ross, and Conrad R. Chao. Cardiovascular regulation and expressions of NO synthase-tyrosine hydroxylase in nucleus tractus solitarius of ovine fetus. Am J Physiol Heart Circ Physiol 284: H1057-H1063, 2003. First published December 5, 2002; 10.1152/ajpheart.00718.2002The purpose of this study was to examine cardiovascular responses to fourth cerebral ventricle (4V) administration of nitroglycerin (NTG) or an inhibitor of nitric oxide (NO) synthase (NOS) in the near-term ovine and to determine whether, during birth, neuronal NOS (nNOS) is induced in noradrenergic A1 neurons in the medial nucleus tractus solitarius (mNTS). In chronically instrumented fetal sheep, 4V injection of NTG (1.2 nmol), an NO donor, produced an arterial blood depressor and a moderate decrease in heart rate. Arterial blood pressure is increased by 4V administration of N G -nitro-Larginine methyl ester (10 nmnol), an inhibitor of NOS, in fetuses. Sections of the medulla from fetuses and newborn lambs were examined by using immunolabeling with tyrosine hydroxylase (TH) antibody combined with NADPH diaphorase (NADPHd) histochemistry, a marker of nNOS activity. The NADPHd-positive cells and TH-positive cells containing NADPHd reactivity were significantly increased in the mNTS of newborns compared with the fetuses. The results suggest that during birth, there is upregulation of NADPHd/nNOS in the noradrenergic neurons of mNTS resulting in a centrally mediated reduction of fetal arterial blood pressure. neuronal nitric oxide synthase; fetal arterial blood pressure; noradrenergic neurons in nucleus tractus solitarius TRANSITION FROM FETAL TO NEWBORN life is accompanied by a marked rise in circulating norepinephrine (NE) concentrations in both animals (12, 23, 24) and infants (11,14,15). However, there is no significant change in arterial blood pressure associated with this dramatic rise in circulating NE during transition (23,24,30). The mechanism for this fetal/neonatal regulation of arterial pressure in response to circulating NE is not known. It has been demonstrated that the central nervous system, particularly the medulla, is responsible for regulation of normal cardiovascular function in fetal lambs (6). The nucleus tractus solitarius (NTS) is the principal sensory nucleus for central regulation of cardiovascular function (1, 32).Recent studies (8,27) have shown that nitric oxide (NO) in the NTS plays an important role in the central inhibition of sympathetic tone and thus decreases arterial blood pressure. Microinjections of nitroglycerin (NTG), an NO donor, into the NTS produce hypotension and bradycardia (19,20), and L-arginine-derived NO directly affects the activity of central autonomic neurons in the NTS (16). Neuronal NO synthase (nNOS), which catalyses the transformation of arginine to NO, is functionally regulated and induced in neurons in the brain (5, 29). We have recently observed that nNOS immunoreactivity and NADPH diaphorase (NADPHd) reactivity are predominately enhanced in th...

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Nitric oxide (NO) modulates the neurogenic control of blood pressure in rats with chronic renal failure (CRF).

Cited by 95 publications

References 56 publications

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

Protective actions of estrogen on angiotensin II-induced hypertension: role of central nitric oxide

Sympathetic Activation in Chronic Renal Failure

Cardiovascular regulation and expressions of NO synthase-tyrosine hydroxylase in nucleus tractus solitarius of ovine fetus

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