Cardiorespiratory reflex control in rats with left ventricular dysfunction

Jung, Ranu; Dibner-Dunlap, Mark E.; Gilles, Maria; Thames, Marc D.

doi:10.1152/ajpheart.1995.268.1.h218

Cited by 11 publications

(14 citation statements)

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“…Thus our results confirm a role for the AV3V region in the abnormal baroreflex response after MI, but suggest that it is not the only factor involved. In HF, both central (18) and peripheral (10) components of the baroreflex activity are said to be impaired.…”

Section: Discussionmentioning

confidence: 99%

Forebrain-mediated adaptations to myocardial infarction in the rat

Francis¹,

Wei²,

Weiß³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Recent studies suggest that the forebrain contributes to the circulatory derangements leading to heart failure after myocardial injury. We tested that hypothesis by examining the effect of myocardial infarction (MI) or sham MI (MI-s) on neurohumoral regulation in rats with prior anteroventral (AV) third ventricle lesion (AV3V-x) or sham lesion (AV3V-s). AV3V-s/MI rats had higher sodium intake, lower urine volume, and lower urinary sodium excretion than AV3V-s/MI-s rats. AV3V-x/MI rats had lower sodium intake and higher urine volume than AV3V-s/MI or AV3V-s/MI-s rats and urinary sodium excretion comparable to AV3V-s/MI-s rats. AV3V-x had no effect on baseline plasma renin activity (PRA). One week after MI, PRA had increased in AV3V-s but decreased in AV3V-x rats. AV3V-x reduced renal sympathetic nerve activity in MI and MI-s rats. AV3V-x improved baroreflex function in MI rats but diminished it in MI-s rats. Survival beyond 2 wk was lower in the AV3V-x/MI rats than in all other groups. These results confirm a critical role for the forebrain in the neurohumoral adjustments to MI.anteroventral third ventricle; baroreflex; sympathetic drive; volume regulation; plasma renin activity CONGESTIVE HEART FAILURE (HF) is characterized by fluid accumulation, increased sympathetic drive, and altered baroreflex regulation (31). These homeostatic abnormalities can be mimicked in normal rats by activating forebrain angiotensin (ANG) type 1 receptors. Blood-borne ANG II, acting via ANG type 1 receptors in the circumventricular organs (CVOs) surrounding the anterior third ventricle, stimulates thirst and sodium appetite, initiates the release of the antidiuretic and vasoconstrictor peptide arginine vasopressin, contributes to sympathetic activation (7,17,24), and modulates baroreflex regulation (2). These influences of blood-borne ANG II can be blocked by a lesion in the anteroventral (AV) third ventricle (AV3V) region (7), which interrupts the descending pathways from forebrain CVOs and from median preoptic nucleus to critical hypothalamic effector neurons.In the rat model of ischemia-induced HF, the activity within one of these effector sites, the paraventricular nucleus of the hypothalamus, is increased, suggesting that this region of the brain is either contributing to or reacting to the development of the HF syndrome. Paraventricular nucleus neurons respond to ascending inputs from brain stem regions that process afferent signals from chemosensitive and mechanosensitive receptors in the cardiovascular system and to descending inputs from CVO neurons stimulated by circulating neuropeptides like ANG II. In HF, both the ascending and the descending systems impinging on the forebrain are altered.The present study examined the effect of a lesion in the AV3V region on neurohumoral mechanisms leading to HF after myocardial infarction (MI) in rats. The hypothesis was that activation of forebrain regions regulating fluid balance and sympathetic drive contributes to the progression of heart failure after MI. In normal rats, the AV3V l...

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Section: Discussionmentioning

confidence: 99%

Forebrain-mediated adaptations to myocardial infarction in the rat

Francis¹,

Wei²,

Weiß³

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…In a clinical study, the assessment of BRS is useful for post infarction risk stratification of worsening hemodynamic state and prognosis. 29 In rats with MI, impaired arterial baroreflex function has been shown, but the mechanism has not been clarified, 16,18 although recent studies suggest that endogenous angiotensin II is a likely candidate. 19,30,31 Some studies have also documented ET actions on BRS 32,33 and those results are controversial because both inhibitory and facilitatory actions have been demonstrated.…”

Section: Discussionmentioning

confidence: 99%

“…A straight line was fitted to the linear portion of the MAP vs RSNA (RSNA was expressed as the percent change from basal nerve activity) curve using regression analysis. 16 The beginning of the linear portion was determined as the MAP value at witch the response for 2 consecutive points had decreased by >5%, and the end of the linear portion was determined as the MAP value at which the response for 2 consecutive points had decreased by <5%. The slope obtained from the RSNA (%) vs MAP (mmHg) curve were used as the arterial BRS.…”

Section: Sympathetic Response Studymentioning

confidence: 99%

Acute Effect of Endothelin AB Antagonist on Sympathetic Outflow in Conscious Rats With Heart Failure.

Tsuchiyama

Kasamatsu

Hano

et al. 2002

Circ J

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ndothelin (ET) is a vasoconstrictor peptide thatgreatly increases the contractility of vascular smooth muscle in pathological and physiological states. 1,2 Recent studies have shown that myocardial and plasma ET concentrations are elevated in congestive heart failure (HF), and increased endogenous ET plays a role in the progression of HF by induction of hypertrophy in cardiomyocytes and left ventricular dilatation. 3 Furthermore, long-term inhibition by the administration of ET A and AB receptor antagonist improves the survival, hemodynamic parameters, and ventricular remodeling in animals with HF. [4][5][6] However, the role of this peptide acting on the autonomic nervous system in HF remains unknown. Sympathoexcitation is well documented in both clinical and experimental HF, and plasma norepinephrine is an entirely independent predictor of mortality in patients with HF. 7-9 It has been reported that exogenous ET promotes sympathetic activation at several loci, including the central nervous system, in the normal animal. 10,11 Thus, it is possible that increased endogenous ET also contributes to this abnormality in HF, and sympathoexcitation via increased ET may be associated with the harmful effect in the progression of HF. However, only 2 studies to our knowledge have shown this phenomenon in the HF state. 12,13 In a recent study, Liu et al Circulation Journal Vol.66, September 2002 showed that the chronic dual ET-1 blockade, L-754, 142, reduced sympathetic activity and normalized the desensitized arterial baroreflex function in another model of experimental HF induced by pacing in rabbits. 14 We hypothesized that ET blockade also reduces the sympathoexcitation in the HF associated with myocardial infarction (MI) and observed the effects of the ET AB dual antagonist, TAK044, on sympathetic outflow and arterial baroreflex sensitivity (BRS) in a conscious rat model of this condition. Methods SubjectsAll procedures were in accordance with institutional guidelines for animal research. Male Wistar rats (n=14, 8 weeks old) were used as the experimental subjects. MI rats were produced by left coronary artery ligation, using techniques similar to those described previously, under intraperitoneal sodium pentobarbital anesthesia. 5 Rats with autopsy-proven transmural MI of the left ventricle were designated as MI rats. The rats were allowed access to their respective drinking water and standard rat chow ad libitum. We used 7 rats with MI at autopsy and elevated left ventricular (LV) end-diastolic pressure (EDP) ≥10 mmHg as models of HF (n=7). We also prepared 7 sham-operated rats (Sham) to compare all data with the HF group. Shams received left side open chest surgery without coronary ligation. All experiments were carried out 6 weeks after ligation. Although ET-1 antagonists have been beneficial in the treatment of heart failure (HF), their involvement in the effect on the sympathetic nervous system in HF remains unknown. The present study investigated the role of endogenous endothelin (ET) in the sympathetic nervou...

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“…paraventricular nucleus; N-methyl-D-aspartic acid receptors; sympathetic nerve activity A CHARACTERISTIC FEATURE of heart failure (HF) is increased sympathoexcitation, which correlates with the severity of the disease as well as complications and mortality (28). The source of the increased sympathoexcitation associated with HF is not entirely understood, although several lines of evidence point to a role for the central nervous system (4,16,19). Sinoaortic (4) or cardiovagal (19) denervation does not normalize plasma norepinephrine (NE) levels in denervated compared with intact HF dogs.…”

mentioning

confidence: 99%

“…The source of the increased sympathoexcitation associated with HF is not entirely understood, although several lines of evidence point to a role for the central nervous system (4,16,19). Sinoaortic (4) or cardiovagal (19) denervation does not normalize plasma norepinephrine (NE) levels in denervated compared with intact HF dogs.…”

mentioning

confidence: 99%

Exercise training normalizes enhanced glutamate-mediated sympathetic activation from the PVN in heart failure

Kleiber

Zheng

Schultz

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kleiber AC, Zheng H, Schultz HD, Peuler JD, Patel KP. Exercise training normalizes enhanced glutamate-mediated sympathetic activation from the PVN in heart failure. Am J Physiol Regul Integr Comp Physiol 294: R1863-R1872, 2008. First published April 2, 2008 doi:10.1152/ajpregu.00757.2007.-Exercise training (ExT) normalizes the increased sympathetic outflow in heart failure (HF), but the mechanisms are not known. We hypothesized that ExT would normalize the augmented glutamatergic mechanisms mediated by N-methyl-D-aspartic acid (NMDA) receptors within the paraventricular nucleus (PVN) that occur with HF. Four groups of rats were used: 1) sham-operated (Sham) sedentary (Sed), 2) Sham ExT, 3) HF Sed, and 4) HF ExT. HF was induced by left coronary artery ligation, and ExT consisted of 3 wk of treadmill running. In ␣-chloralose-urethaneanesthetized rats, the increase in renal sympathetic nerve activity in response to the highest dose of NMDA (200 pmol) injected into the PVN in the HF Sed group was approximately twice that of the Sham Sed group. In the HF ExT group the response was not different from the Sham Sed and Sham ExT groups. Relative NMDA NR1 receptor subunit mRNA expression was 63% higher in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not different from the Sham Sed and Sham ExT groups. NR1 receptor subunit protein expression was increased 87% in the HF Sed group compared with the Sham Sed group but in the HF ExT group was not significantly different from the Sham Sed and Sham ExT groups. Thus one mechanism by which ExT alleviates elevated sympathetic outflow in HF may be through normalization of glutamatergic mechanisms within the PVN. paraventricular nucleus; N-methyl-D-aspartic acid receptors; sympathetic nerve activity A CHARACTERISTIC FEATURE of heart failure (HF) is increased sympathoexcitation, which correlates with the severity of the disease as well as complications and mortality (28). The source of the increased sympathoexcitation associated with HF is not entirely understood, although several lines of evidence point to a role for the central nervous system (4,16,19). Sinoaortic (4) or cardiovagal (19) denervation does not normalize plasma norepinephrine (NE) levels in denervated compared with intact HF dogs. Plasma NE is also not altered in HF dogs by ␤-adrenergic blockade (19). Stimulation of the aortic depressor nerve produces altered lumbar sympathetic nerve activity in rats with HF compared with sham-treated rats (16). Together these data indicate an alteration within the central nervous system in HF.The paraventricular nucleus (PVN) of the hypothalamus is reciprocally connected to other areas of the brain involved in control of cardiovascular function (18) and contains preautonomic neurons that project to sympathetic preganglionic neurons within the intermediolateral cell column of the spinal cord both directly and indirectly via the rostral ventrolateral medulla (40). Previous data from this laboratory suggest that the increased activity of PVN neurons ass...

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Cardiorespiratory reflex control in rats with left ventricular dysfunction

Cited by 11 publications

References 0 publications

Forebrain-mediated adaptations to myocardial infarction in the rat

Forebrain-mediated adaptations to myocardial infarction in the rat

Acute Effect of Endothelin AB Antagonist on Sympathetic Outflow in Conscious Rats With Heart Failure.

Exercise training normalizes enhanced glutamate-mediated sympathetic activation from the PVN in heart failure

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