Angiotensin II receptors in the solitary-vagal area of hypertensive rats.

Healy, Dennis P.; Zhang, Nan

doi:10.1161/01.hyp.19.4.355

Cited by 16 publications

(14 citation statements)

References 32 publications

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“…After DOCA-salt treatment for 1 month, renin-like activity and Ang II in hypothalamus and brain stem nuclei were elevated, but plasma renin activity was very low (7,8). In rats with DOCA-salt hypertension for 4-8 weeks, angiotensin II receptor binding on autoradiography was also elevated in selected brain areas involved in cardiovascular regulation, such as nucleus of solitary tract, area postrema, median preoptic nucleus, subfornical organ, and solitary vagal area (4)(5)(6). Moreover, BP responses to centrally administered Ang II were significant- (4,25).…”

Section: Discussionmentioning

confidence: 99%

“…DOCA-salt-treated rats show higher Ang II receptor density in brain areas involved in cardiovascular regulation, such as the nucleus of solitary tract, area postrema, median preoptic nucleus, subfornical organ, and solitary vagal area (4)(5)(6), and have elevated levels of renin and Ang II in hypothalamus and brain stem nuclei (7,8). Acute intracerebroventricular (icv) administration of captopril decreases the blood pressure of DOCA-salt hypertensive rats (9).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Centrally Administered Losartan on Deoxycorticosterone-salt Hypertension Rats

Park

Leenen

2001

J Korean Med Sci

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INTRODUCTIONIn deoxycorticosterone acetate (DOCA)-salt hypertensive rats the development and maintenance of hypertension is considered to be independent of the renin-angiotensin system, because plasma renin in this model is low (1), and peripheral administration of angiotensin converting enzyme (ACE) inhibitors (2) or angiotensin (Ang) II receptor antagonists (3) has no effect on blood pressure (BP). However, there is some evidence for a role of the brain renin-angiotensin system in the pathogenesis of DOCA-salt hypertension in rats.DOCA-salt-treated rats show higher Ang II receptor density in brain areas involved in cardiovascular regulation, such as the nucleus of solitary tract, area postrema, median preoptic nucleus, subfornical organ, and solitary vagal area (4-6), and have elevated levels of renin and Ang II in hypothalamus and brain stem nuclei (7,8). Acute intracerebroventricular (icv) administration of captopril decreases the blood pressure of DOCA-salt hypertensive rats (9). Chronic icv administration of captopril attenuates the development of hypertension in DOCA-salt hypertensive rats (10). However, the interpretation of these findings is complicated because ACE is involved in the metabolism of various peptides that may participate in regulating BP, including bradykinin, enkephalin and substance P (11).Three studies assessed the effects of icv Ang II receptor antagonists on BP in DOCA-salt hypertensive rats. Acute icv administration of salarasin did not lower BP during 30 min of follow-up (12). In contrast, injection of losartan icv or into the rostral part of the third ventricle did lower BP for more than 1 hr in 4 weeks DOCA-salt hypertensive rats (13). Moreover, continuous icv infusion of CV-11974 (active metabolite of candesartan) for 7 days lowered BP from the fourth day after infusion (14). However, because hemodynamic measurements in these studies were done under anesthesia in 4 weeks and 6 weeks DOCA-salt hypertensive rats, the role of brain Ang II in the development of the hypertension in the DOCA-salt hypertensive rat model is not known yet.The aim of the present study was to determine the acute central effects of the type 1 Ang II (AT1) receptor antagonist losartan in conscious DOCA-salt hypertensive rats, at either 2 weeks during the development of the hypertension or at 4 weeks in the maintenance phase of the hypertension. MATERIALS AND METHODS AnimalsMale Wistar rats aged 5 weeks, weighing 140-170 g, were J Korean Med Sci 2001; 16: 553-7 ISSN 1011-8934 Copyright � The Korean Academy of Medical Sciences 553 Effects of Centrally Administered Losartan on Deoxycorticosteronesalt Hypertension RatsTo investigate whether brain AT1 receptor stimulation contributes as a hypertensive mechanism to deoxycorticosterone acetate (DOCA)-salt hypertension, losartan (1 mg/4 L) or artificial cerebrospinal fluid (aCSF) was injected into the lateral cerebral ventricle in conscious control uninephrectomized Wistar rats or rats with DOCA-salt for 2 or 4 weeks, and mean arterial pressure (MAP) and heart r...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Centrally Administered Losartan on Deoxycorticosterone-salt Hypertension Rats

Park

Leenen

2001

J Korean Med Sci

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“…6 -10 Furthermore, there appear to be alterations in SHR in the amount of angiotensin or its receptors in discrete brain regions. 3,4,11,12 Despite this important role of brain Ang II in hypertension, the site (or sites) within the brain at which Ang II acts in this regard is not fully worked out. Certainly, Ang II can act within the hypothalamus to influence cardiovascular regulation.…”

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confidence: 99%

Ventrolateral Medulla AT ₁ Receptors Support Blood Pressure in Hypertensive Rats

et al. 2002

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Abstract-Angiotensin within the central nervous system appears to be important for the maintenance of hypertension in spontaneously hypertensive rats. This study addresses the hypothesis that blockade of AT 1 receptors in the rostral ventrolateral medulla would decrease blood pressure in spontaneously hypertensive rats and that this tonically active AT 1 -mediated input to the rostral ventrolateral medulla arises from the hypothalamic paraventricular nucleus. Injection of the nonpeptide AT 1 receptor antagonist valsartan bilaterally into the rostral ventrolateral medulla of choralose-anesthetized adult spontaneously hypertensive rats produced a dose-related decrease in mean arterial pressure, with a maximal effect of Ϸ30 mm Hg. Inhibition of the paraventricular nucleus by local injection of muscimol elicited a similar response, which was inhibited by prior injection of valsartan into the rostral ventrolateral medulla. In contrast, in control Wistar-Kyoto rats, neither valsartan injected into the rostral ventrolateral medulla nor muscimol injected into the paraventricular nucleus had a substantial effect on arterial pressure. These data indicate that in spontaneously hypertensive rats but not in Wistar-Kyoto rats, rostral ventrolateral medulla vasomotor neurons are tonically excited by endogenous stimulation of AT 1 receptors, and this input is apparently driven from the hypothalamus. These results suggest that the rostral ventrolateral medulla is one site that the brain renin-angiotensin system acts to maintain elevated blood pressure in spontaneously hypertensive rats. The data supporting of a role of brain Ang II in hypertension in the spontaneously hypertensive rats (SHR) are particularly convincing. Specifically, pharmacological disruption of brain angiotensin signaling decreases AP in SHR. 6 -10 Furthermore, there appear to be alterations in SHR in the amount of angiotensin or its receptors in discrete brain regions. 3,4,11,12 Despite this important role of brain Ang II in hypertension, the site (or sites) within the brain at which Ang II acts in this regard is not fully worked out. Certainly, Ang II can act within the hypothalamus to influence cardiovascular regulation. 13 However, Ang II can also act in the caudal brain stem to increase AP and sympathetic outflow. 14 One region in the caudal brain stem that probably mediates some of the central cardiovascular effects of Ang II is the rostral ventrolateral medulla (RVLM). 15,16 The RVLM appears to be the brain site responsible for the maintenance of basal sympathetic vasomotor activity, and inhibition of RVLM neurons reduces AP to the same extent as total inhibition of sympathetic vasomotor activity. Conversely, stimulation of neurons in the RVLM increases AP. There is evidence that increased activity of the RVLM supports the elevated AP in SHR. [17][18][19] The RVLM also has a high density of angiotensin AT 1 receptors. 20 Furthermore, microinjection of Ang II into the RVLM increases AP and sympathetic nerve activity, [21][22][23][24] and stimulation of A...

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“…Exaggerated angiotensin-mediated 27 synaptic transmission at the caudal NTS was demonstrated in hypertensive animals, along with an increase in the density of angiotensin receptors in the caudal NTS. 28 It follows that our identified causative relationship among Ang II, AT 1 R, and Fos expression at the caudal NTS represents a subtle cascade of intracellular events to ensure that the octapeptide may exert a long-term inhibitory modulation on beat-to-beat BRR control of blood pressure. An exaggeration of this linkage may lead to further impairment of the BRR response during hypertension.…”

Section: Luoh and Chan C-fos And Baroreflex Inhibition By Angiotensinmentioning

confidence: 87%

Inhibition of Baroreflex by Angiotensin II via Fos Expression in Nucleus Tractus Solitarii of the Rat

Luoh

Chan

2001

Hypertension

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Abstract-We evaluated the modulatory action of angiotensin II at the nucleus tractus solitarii on spontaneous baroreceptor reflex response, the angiotensin subtype receptors involved, and the role of Fos protein in this process, using Sprague-Dawley rats anesthetized with pentobarbital sodium. Microinjection bilaterally of angiotensin (Ang ) II (5, 10, 20, or 40 pmol) into the nucleus tractus solitarii significantly suppressed the spontaneous baroreceptor reflex, as represented by the magnitude of transfer function between systemic arterial pressure and heart rate signals. There also was a concomitant increase in Fos-like immunoreactivity in the nucleus tractus solitarii. Both the suppression of spontaneous baroreceptor reflex and Fos expression in nucleus tractus solitarii neurons elicited by Ang II were discernibly attenuated by pretreatment with or comicroinjection into the bilateral nucleus tractus solitarii of a 15-mer antisense c-fos oligonucleotide that targets against the initiation codon of c-fos mRNA. In addition, those 2 actions of Ang II were reversed by the coadministration of the nonpeptide Ang II type 1 (AT 1 ) receptor antagonist losartan (1.6 nmol) but not by the nonpeptide AT 2 receptor antagonist PD 123,319 (1.6 nmol).

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Angiotensin II receptors in the solitary-vagal area of hypertensive rats.

Cited by 16 publications

References 32 publications

Effects of Centrally Administered Losartan on Deoxycorticosterone-salt Hypertension Rats

Effects of Centrally Administered Losartan on Deoxycorticosterone-salt Hypertension Rats

Ventrolateral Medulla AT ₁ Receptors Support Blood Pressure in Hypertensive Rats

Inhibition of Baroreflex by Angiotensin II via Fos Expression in Nucleus Tractus Solitarii of the Rat

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Angiotensin II receptors in the solitary-vagal area of hypertensive rats.

Cited by 16 publications

References 32 publications

Effects of Centrally Administered Losartan on Deoxycorticosterone-salt Hypertension Rats

Effects of Centrally Administered Losartan on Deoxycorticosterone-salt Hypertension Rats

Ventrolateral Medulla AT 1 Receptors Support Blood Pressure in Hypertensive Rats

Inhibition of Baroreflex by Angiotensin II via Fos Expression in Nucleus Tractus Solitarii of the Rat

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Ventrolateral Medulla AT ₁ Receptors Support Blood Pressure in Hypertensive Rats