Acute and chronic angiotensin hypertension: neural and nonneural components, time course, and dose dependency

Li, Q.; Dale, William E.; Hasser, Eileen M.; Blaine, Edward H.

doi:10.1152/ajpregu.1996.271.1.r200

Cited by 60 publications

(92 citation statements)

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“…Blood-borne Ang II is known to produce a long-term hypertensive response by both peripheral and brain mechanisms [20][21] . Since the hypertensive effect of combined treatment with Ang II and TMAO appeared after 5 days of infusions, it may be hypothesized that the effect was caused rather by long-term Ang II-dependent mechanisms such as an increase in blood volume or an increase in sympathetic drive due to the activation of central mechanisms involved in BP control 13,21 .…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

“…Since the hypertensive effect of combined treatment with Ang II and TMAO appeared after 5 days of infusions, it may be hypothesized that the effect was caused rather by long-term Ang II-dependent mechanisms such as an increase in blood volume or an increase in sympathetic drive due to the activation of central mechanisms involved in BP control 13,21 . This notion may also be supported by our preliminary experiments in which we found that short, 30-seconds-long IV infusions of TMAO at a dose of 1 to 12 mmol × s -1 did not affect resting BP and hypertensive effects of Ang II in rats (data not presented).…”

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

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Trimethylamine-N-Oxide: A Carnitine-Derived Metabolite That Prolongs the Hypertensive Effect of Angiotensin II in Rats

Ufnal

Jaźwiec

Dadlez

et al. 2014

Canadian Journal of Cardiology

185

130

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Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Section: A C C E P T E D Accepted Manuscriptmentioning

confidence: 99%

Trimethylamine-N-Oxide: A Carnitine-Derived Metabolite That Prolongs the Hypertensive Effect of Angiotensin II in Rats

Ufnal

Jaźwiec

Dadlez

et al. 2014

Canadian Journal of Cardiology

185

130

View full text Add to dashboard Cite

“…To address this question, we used intravenous administration of a hypertensive concentration of ANG II and ganglionic blockade with trimetaphan because these techniques have been previously used to evaluate the contribution of SNS stimulation to the pressor response evoked by ANG II (6,25).…”

mentioning

confidence: 99%

“…Systemic ANG II has been implicated in chronically increased blood pressure through several mechanisms, including activation of the SNS (25,48). Although the initial increase in blood pressure during peripheral administration of pressor concentrations of ANG II is due to the direct vasoconstrictor effects of the hormone on vascular smooth muscle, the chronic hypertensive response to longer-term, continuous administration (hours to days) of ANG II is mediated by progressive activation of the SNS (6,25).…”

mentioning

confidence: 99%

“…Although the initial increase in blood pressure during peripheral administration of pressor concentrations of ANG II is due to the direct vasoconstrictor effects of the hormone on vascular smooth muscle, the chronic hypertensive response to longer-term, continuous administration (hours to days) of ANG II is mediated by progressive activation of the SNS (6,25). Indeed, a predominant mechanism through which ANG II contributes to sustained hypertension is activation of central SNS sympathoexcitatory centers (11).…”

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Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion

Bealer

2003

American Journal of Physiology-Heart and Circulatory Physiology

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Bealer, Steven L. Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion. Am J Physiol Heart Circ Physiol 284: H559-H565, 2003. First published October 24, 2002 10.1152/ajpheart.00628.2002Increased dietary sodium enhances both excitatory and inhibitory blood pressure responses to stimulation of the central sympathetic nervous system (SNS) centers. In addition, long-term (hours to days) administration of ANG II increases blood pressure by activation of the SNS. These studies investigated the effects of increased dietary sodium on SNS control of blood pressure during 0-to 24-h infusion of ANG II in conscious, male rats consuming either tap water or isotonic saline (Iso) for 2 to 3 wk. The SNS component (evaluated by ganglionic blockade with trimetaphan) of both control blood pressure and the pressor response to intravenous ANG II was reduced in Iso animals. Furthermore, although the pressor response to intravenous ANG II infusion was similar between groups, the baroreflexinduced bradycardia during the initial 6 h of ANG II infusion was significantly greater, whereas the tachycardia accompanying longer infusion periods was significantly attenuated in Iso animals. These data suggest that in normal rats increased dietary sodium enhances sympathoinhibitory responses during intravenous ANG II. baroreflex; heart rate; sympathoexcitation; sympathoinhibition; hypertension INCREASED DIETARY SODIUM has been associated with the enhanced risk of high blood pressure (4, 12) because increased salt intake induces and/or increases hypertension in several experimental animal models (1,15,34,40). However, the mechanisms of the hypertensinogenic effects of increased dietary sodium have not been completely defined. Several studies (37,38,47) have suggested that elevated sodium ingestion is associated with activation of the sympathetic nervous system (SNS), and it has been proposed that increasing dietary salt alters the SNS circuits that regulate SNS control of cardiovascular function (37,41).In support of this proposal, recent studies (19, 39) show that animals on a high-salt diet demonstrate enhanced pressor responses to microinjection of several excitatory neurotransmitters into the rostral ventrolateral medulla. These authors suggest that although dietary sodium does not increase blood pressure alone, it may contribute to development of hypertension by potentiating the actions of other hypertensive stimuli on SNS centers. However, in addition to enhancing sympathoexcitatory responses to stimulation of medullary pressor sites, increased dietary sodium also potentiates the depressor responses to both glutamate injections in the nucleus tractus solitarius (19) and aortic nerve stimulation (39) and enhances baroreflex-induced bradycardia (39). Therefore, it appears that both sympathoexcitatory and sympathoinhibitory responses are sensitized by increased dietary sodium. However, the physiological significance of these observations has not been completely defined.Systemic ANG II has been im...

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Renal sympathetic nerve activity in the development of hypertension

Malpas

Ramchandra²,

Guild³

et al. 2006

Current Science Inc

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With increasing evidence that the sympathetic nervous system plays a critical role in the development of hypertension, focus is turning to how these signals translate to a chronic increase in arterial pressure. The kidney's role in the control of salt and water homeostasis makes it an obvious target for such investigations. However, to date many studies have been restricted to experiments that last only a few hours, or at most, a few days, whereas others may use indirect methods of assessing sympathetic activity rather than direct recordings. We review current approaches used to determine the effects of renal sympathetic nerve activity (SNA) on arterial pressure and suggest possible avenues of future investigation. We propose that although afferent inputs, such those as from chemoreceptors and baroreceptors, are important for the short-term control of blood pressure via regulation of SNA to multiple organs, it is highly likely that alternative signals are important for setting the long-term level of renal SNA. Emerging evidence indicates that circulating angiotensin II is a hormone that may act on the central nervous system to regulate renal SNA, renal function, and, therefore, blood pressure. Future studies on the genesis of hypertension should focus more on determining the mediators of long-term levels of renal SNA.

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Acute and chronic angiotensin hypertension: neural and nonneural components, time course, and dose dependency

Cited by 60 publications

References 0 publications

Trimethylamine-N-Oxide: A Carnitine-Derived Metabolite That Prolongs the Hypertensive Effect of Angiotensin II in Rats

Trimethylamine-N-Oxide: A Carnitine-Derived Metabolite That Prolongs the Hypertensive Effect of Angiotensin II in Rats

Increased dietary sodium alters neural control of blood pressure during intravenous ANG II infusion

Renal sympathetic nerve activity in the development of hypertension

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