Cardiac sympathetic overactivity and decreased baroreflex sensitivity in <scp>l</scp>-NAME hypertensive rats

Souza, Hugo Celso Dutra de; Ballejo, Gustavo; Salgado, Maria Cristina de Oliveira; Silva, Valdo José Dias da; Salgado, Hélio César

doi:10.1152/ajpheart.2001.280.2.h844

Cited by 64 publications

(65 citation statements)

References 42 publications

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“…31,32 In L-NAME-hypertensive rats, both a decrease and an increase in baroreflex sensitivity have been reported. 28,30,33 NO synthesis in mice resulted in an enhancement of baroreflex sensitivity in an earlier study. 31 In our study, L-NAME treatment increased blood pressure to a greater degree in AT 2 Ϫ/Ϫ than in controls, suggesting an augmented sensitivity of AT 2 Ϫ/Ϫ mice to L-NAME.…”

Section: Discussionmentioning

confidence: 81%

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Heart Rate Variability and Baroreflex Function in AT ₂ Receptor-Disrupted Mice

et al. 2002

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Abstract-We adapted telemetry and sequence analysis employed in humans to mice and measured heart rate variability and the spontaneous baroreflex sensitivity in angiotensin II type 2 (AT 2 ) receptor-deleted (AT 2 Ϫ/Ϫ) and wild-type (AT 2 ϩ/ϩ) mice with either deoxycorticosterone acetate (DOCA)-salt hypertension or N-nitro-L-arginine methylester hydrochloride (L-NAME) hypertension. Mean arterial pressure leveled during the day at 101Ϯ1 mm Hg and during the night at 109Ϯ1 mm Hg in AT 2 receptor-deleted mice, compared with 98Ϯ2 mm Hg (day) and 104Ϯ2 mm Hg (night) in wild-type mice. Mean arterial pressure increased in AT 2 receptor-deleted mice with L-NAME to 114Ϯ1 mm Hg (day) and 121Ϯ1 mm Hg (night), compared with 105Ϯ2 mm Hg (day) and 111Ϯ2 mm Hg (night), respectively. DOCA-salt also increased day and night blood pressures in AT 2 receptor-deleted mice to a greater degree than in wild-type mice. Heart rate variability in the time and frequency domain was not different between AT 2 receptor-deleted mice and AT 2 receptor-deleted mice at baseline. Systolic blood pressure variability in the low frequency band was lower in AT 2 receptor-deleted mice (0.6Ϯ0.1 ms 2 versus 3.9Ϯ1.3 ms 2 ) than in wild-type mice. Baroreceptor-heart rate reflex sensitivity was significantly increased in AT 2 receptor-deleted mice compared with wild-type mice (3.4Ϯ0.6 versus 2.1Ϯ0.5 ms/mm Hg). These differences remained after DOCA-salt and L-NAME treatments. We conclude that activation of the AT 2 receptor impairs arterial baroreceptor reflex function, probably by a central action. These data support the existence of an inhibitory central effect of the AT 2 receptor on baroreflex function. Although not yet as clearly delineated as the AT 1 receptor, the AT 2 receptor may be responsible for counterregulating the effects induced by the AT 1 receptor. 1 In accord with this view, disruption of the AT 2 receptor caused increased blood pressure in mice and increased vasopressor responses to Ang II. [1][2][3][4][5] In experimental and human hypertension, the sensitivity of the baroreceptor control of heart rate is reduced and has been associated with an overactivity of the renin-angiotensin system. 6 Endogenous Ang II affects the baroreceptor function through the AT 1 receptor 7,8 and the AT 2 receptor via central tonic inhibitory effects. 9,10 Therefore, the AT 2 receptor gene-disrupted (Ϫ/Ϫ) mouse could be a useful model for studying the involvement of the AT 2 receptor in baroreceptor function. In man, the combined computer analysis of spontaneous blood pressure and heart rate fluctuations allows the assessment of baroreflex function without invasive or provocative interventions. We adapted telemetry to AT 2 receptor Ϫ/Ϫ and wild-type (ϩ/ϩ) mice to study blood pressure and continuous spontaneous baroreflex function in the mouse. To our knowledge, this report is the first in which these clinically accepted methods are applied to mice. MethodsExperiments were performed on 8 adult male AT 2 receptor-deleted (AT 2 Ϫ/Ϫ) and 7 male wild-type (AT 2 ϩ/...

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Section: Discussionmentioning

confidence: 81%

“…28 These observations prompted us to investigate baroreceptor function in L-NAME hypertensive mice with blocked NO synthesis and to compare these mice with DOCA-salt hypertensive mice. In DOCA-salt hypertensive mice, the NO system is stimulated.…”

Section: Discussionmentioning

confidence: 99%

Heart Rate Variability and Baroreflex Function in AT ₂ Receptor-Disrupted Mice

et al. 2002

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“…6 The data is relevant since baroceptor reflex is largely studied in different models and strains of rats aiming to prevent hypertension development in humans 12,27-29 , because reduced baroreflex function is indicative of cardiovascular disease. [30][31][32][33] In conclusion, we found differences of baroreflex function among WKY rats. The majority of animals (82%) presented attenuated parasympathetic activity of the baroreflex (reduced bradycardic responses to increase in arterial pressure and reduced baroreflex gain tested with PE) while 22% presented decreased sympathetic activity of the baroreflex (reduced tachycardic responses to decreased arterial pressure and reduced baroreflex gain tested with SNP).…”

Section: Discussionmentioning

confidence: 94%

Intra-strain variations of baroreflex sensitivity in young Wistar-Kyoto rats

Valenti

Imaizumi²,

Abreu³

et al. 2009

CIM

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Clin Invest Med 2009; 32 (6): E251-E257. AbstractPurpose: To compare baroreflex sensitivity among conscious rats of the same strain. Methods: Male WKY rats (eight weeks old) were studied. Cannulas were inserted into the abdominal aortic artery through the right femoral artery to measure mean arterial pressure (MAP) and heart rate (HR). Baroreflex gain was calculated as the ratio between variation of HR in function of the MAP variation (ΔHR/ΔMAP) tested with a depressor dose of sodium nitroprusside (SNP, 50µg/kg, iv) and with a pressor dose of phenylephrine (PE, 8µg/kg, iv). We divided the rats into four groups: 1) Low bradycardic baroreflex (LB), BG between -1 and -2 bpm/mmHg tested with PE; 2) High bradycardic baroreflex (HB), BG < -2 bpm/mmHg tested with PE; 3) Low tachycardic baroreflex (LT), BG between -1 and -2 bpm/mmHg tested with SNP and; 4) High tachycardic baroreflex (HT), BG < -2 bpm/ mmHg tested with SNP. Significant differences were considered for p<0.05.Results: Approximately 82% of the rats presented reduced bradycardic reflex while 22 showed attenuated tachycardic reflex. No alterations were noted regarding basal MAP and HR, tachycardic and bradycardic peak and HR range. Conclusions: There was alteration in baroreflex sensitivity among rats of the same strain. Care should be taken when interpreting studies employing WKY as a control for the SHR.In 1963, Okamoto and Aoki 1 reported that they had selectively bred Wistar rats to be spontaneously hypertensive. Established as an inbred strain in 1969 at the National Institutes of Health (NIH), the spontaneously hypertensive rat (SHR) remains the most widely studied animal model of essential hypertension (i.e., persistent high blood pressure of unknown causation), and the strain presents similar characteristic to hypertension in humans. As controls for the SHR, most workers have employed normotensive descendants of Wistar rats that NIH investigators obtained in 1971 from the colony in Kyoto from which the SHR strain was originally derived (Wistar-Kyoto rats, WKY). 2 Baroreflex function is one of the body's homeostatic mechanisms to sustain arterial pressure. It offers a negative feedback loop in which the increased arterial pressure reflexively causes blood pressure to de-

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“…In addition, they observed tachycardia associated with hypertension induced by sympathetic hyperactivity, no change in intrinsic heart rate. (68) The direct effect of L-NAME preventing endothelial synthesis of NO and reducing the tonic vasodilation is an important mechanism in the genesis of this model experimental hypertension. (69) The pressure in this experimental model was also associated with kidney damage, characterized by glomerulosclerosis, glomerular ischemia and renal interstitial infiltrate.…”

Section: Renopriva Hypertensionmentioning

confidence: 93%

Effects of aerobic exercise training in animal models of hypertension.

Palma¹,

Malfitano²,

Shimojo³

et al. 2015

mtprehabjournal

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Background: Hypertension is one of the leading causes of death due to stroke, heart attack and kidney failure. The understanding of the pathophysiological mechanisms involved in its development and maintenance is critical to potential therapeutic interventions. Thus, animal models of hypertension have been used in the study of this disease for many years. Objective: To investigated the effects of dynamic aerobic exercise training as a non-pharmacological approach for the management of hypertension in animal models. Method/Design: This study is a literature review conducted in the Medline database. Results: The results demonstrated that aerobic exercise training may reduce blood pressure in different rat models of hypertension. Conclusions: The dynamic aerobic exercise can reduced blood pressure in different animal models of hypertension by mechanisms that involving neurohumoral changes, reinforcing the important role of this approach in the treatment of hypertension and its associated disorders.

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Cardiac sympathetic overactivity and decreased baroreflex sensitivity in l-NAME hypertensive rats

Cited by 64 publications

References 42 publications

Heart Rate Variability and Baroreflex Function in AT ₂ Receptor-Disrupted Mice

Heart Rate Variability and Baroreflex Function in AT ₂ Receptor-Disrupted Mice

Intra-strain variations of baroreflex sensitivity in young Wistar-Kyoto rats

Effects of aerobic exercise training in animal models of hypertension.

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Cardiac sympathetic overactivity and decreased baroreflex sensitivity in l-NAME hypertensive rats

Cited by 64 publications

References 42 publications

Heart Rate Variability and Baroreflex Function in AT 2 Receptor-Disrupted Mice

Heart Rate Variability and Baroreflex Function in AT 2 Receptor-Disrupted Mice

Intra-strain variations of baroreflex sensitivity in young Wistar-Kyoto rats

Effects of aerobic exercise training in animal models of hypertension.

Contact Info

Product

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Heart Rate Variability and Baroreflex Function in AT ₂ Receptor-Disrupted Mice

Heart Rate Variability and Baroreflex Function in AT ₂ Receptor-Disrupted Mice