NO and Angiotensin II Effects on Blood Pressure andFluid Homeostasis

Liu, Hanwu; Terrell, Mary Lee; Bui, Vuong; Summy-Long, Joan Y.; Kadekaro, Massako

doi:10.1046/j.1365-2826.1997.00606.x

Cited by 19 publications

(19 citation statements)

References 4 publications

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“…The inhibition of the NO synthesis results in an imbalance between the renin-angiotensin system (RAS) and the NO system in favor of the RAS; thus the effects of ANG II may prevail (20,30). 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).…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

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confidence: 99%

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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%

mentioning

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

View full text Add to dashboard Cite

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“…One possible reason is that NO suppresses the excitatory input to the PVN and SON and causes a reduction in sensitivity to osmotic stimuli in the diabetic state, because NO in the PVN and SON tonically inhibit secretion of AVP and oxytocin [21,22]. Furthermore, diabetes is known to induce changes in the noradreanline and adrenaline concentrations of the various brain regions, including the hypothalamus [1,2].…”

Section: Discussionmentioning

confidence: 99%

“…The magnocellular neurosecretory cells in the PVN and SON synthesize arginine vasopressin (AVP) and oxytocin and release them into the systemic cirulation from their axon terminals located in the posterior pituitary. Some studies have demonstrated that hypothalamic NO inhibits release of AVP [17,19,20] and central NO tonically inhibits basal release of AVP and oxytocin [21,22]. Thus, NO may play an important role in the modulation of secretion of AVP and oxytocin in the hypothalamo-neurohypophysial system [17,19,23].…”

Section: : 640±648]mentioning

confidence: 99%

Upregulation of hypothalamic nitric oxide synthase gene expression in streptozotocin-induced diabetic rats

et al. 1998

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The peripheral administration of streptozotocin (STZ) causes marked hyperglycaemia, plasma hyperosmolality, hypoinsulinaemia, hyperphagia and polydipsia. In STZ-induced diabetic animals, insulin treatment reverses these symptoms. Several studies have demonstrated that insulin deficiency induced diabetes causes alteration of hypothalamic transmitters and the gene expressions of neuropeptides [1±7]. These studies suggest that the alteration of monoamine and neuropeptides in the hypothalamus may play a role in the multiple behavioural and hormonal abnormalities in STZ-induced diabetic rats.Recent studies have demonstrated that nitric oxide (NO) may be associated with various functions of the central nervous system, including feeding [8±12] and drinking behaviour [13,14]. It has been demonstrated that both systemic administration of a competitive antagonist of NO synthase (NOS) and Diabetologia (1998) Summary Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. Four weeks after intraperitoneal (i. p.) administration of STZ, male Wistar rats developed hyperglycaemia and plasma hyperosmolality. The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. [Diabetologia (1998) 41: 640±648]

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“…Almost all studies of NO actions on oxytocin neurons show inhibitory effects. Thus, the NO donor sodium nitroprusside (SNP) and the NO precursor l ‐arginine inhibit SON neurons, whereas NOS inhibitors increase the activity of stimulated oxytocin neurons in vivo (Liu et al. , 1997; Srisawat et al.…”

Section: Introductionmentioning

confidence: 99%

The role of nitric oxide in morphine dependence and withdrawal excitation of rat oxytocin neurons

Bull

Ludwig

Blackburn-Munro

et al. 2003

Eur J of Neuroscience

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Magnocellular oxytocin neurons develop morphine dependence after intracerebroventricular infusion for 5 days as revealed by their profound excitation following naloxone-induced withdrawal. Oxytocin neurons strongly express nitric oxide synthase (NOS) and nitric oxide (NO) inhibits their activity. This study investigated whether excitation of oxytocin neurons during morphine withdrawal involves reduced activity of NOS and NO. Neuron activity was measured in urethane-anaesthetized rats with blood sampling for oxytocin radioimmunoassay and extracellular single unit firing rate recording of supraoptic nucleus oxytocin neurons. To compare morphine-dependent and -naive rats oxytocin secretion was measured during stimulation by intravenous hypertonic saline infusion. Prior treatment with Nomega-nitro-l-arginine methyl ester, a NOS inhibitor, facilitated osmotically stimulated oxytocin secretion in both morphine-dependent and -naive rats. The facilitation was not different between these groups when corrected for the slower responses observed in morphine-dependent rats. Treatment of morphine-dependent rats with Nomega-nitro-l-arginine methyl ester also enhanced oxytocin secretion during naloxone-precipitated withdrawal. Oxytocin neurons excited by withdrawal were recorded during microdialysis application to the supraoptic nucleus of the NO donor sodium nitroprusside alone and in combination with the GABAA antagonist bicuculline. Sodium nitroprusside inhibited oxytocin neurons during naloxone-precipitated morphine withdrawal and, while bicuculline alone increased firing rate, it did not reduce the inhibition by sodium nitroprusside, in contrast with previous findings in naive rats. Together, these findings indicate that NO restraint of oxytocin secretion is not curtailed during morphine dependence and remains a potent inhibitor of withdrawal excitation despite reduced effectiveness on GABA innervation of the supraoptic nucleus. Hence there is no evidence that changes in NO regulation underlie excitation of oxytocin neurons during opiate withdrawal in morphine dependence.

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NO and Angiotensin II Effects on Blood Pressure andFluid Homeostasis

Cited by 19 publications

References 4 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

Upregulation of hypothalamic nitric oxide synthase gene expression in streptozotocin-induced diabetic rats

The role of nitric oxide in morphine dependence and withdrawal excitation of rat oxytocin neurons

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