Acute AT1 receptor blockade does not improve the depressed baroreflex in rats with chronic renal hypertension

Farah, Vera; Moreira, Edson Dias; Ushizima, M.R.; Cestari, Idágene Aparecida; Irigoyen, Maria-Cláudia; Krieger, Eduardo Moacyr

doi:10.1590/s0100-879x2000001200014

Cited by 5 publications

(3 citation statements)

References 18 publications

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“…The first is the operating point of the reflex (i.e., arterial pressure) and the second is the sensitivity of the reflex . The operating point and the sensitivity of the baroreceptor reflex are altered in physiological and pathophysiological situations, such as development , aging , pregnancy , different sleep states , or hypertension . Activation of baroreceptors results in increased firing of action potentials, with the rapidity determined by the degree of mechanical stretch.…”

Section: The Baroreceptor Reflexmentioning

confidence: 99%

Dysautonomic responses during percutaneous carotid intervention

Bujak

Stilp

Meller

et al. 2014

Cathet Cardio Intervent

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Percutaneous carotid artery stenting (CAS) has emerged as a less invasive alternative to carotid endarterectomy for the treatment of carotid atherosclerotic disease. The main risk of CAS is the occurrence of neuro-vascular complications; however, carotid artery stenting-related dysautonomia (CAS-D) (hypertension, hypotension, and bradycardia) is the most frequently reported problem occurring in the periprocedural period. Alterations in autonomic homeostasis result from baroreceptor stimulation, which occurs particularly at the time of balloon inflation in the region of the carotid sinus. The response can be profound enough to induce asystole or even complete cessation of postganglionic sympathetic nerve activity. Frequency and factors predisposing a patient to CAS-D have been investigated in several studies; however, there are significant discrepancies in results among reports. Lack of consistent findings may arise from using different methods and definitions, as well as other factors discussed in detail in this review. Furthermore, a correlation of CAS-D with short and long-term outcomes has been investigated only in small and mostly retrospective studies, explaining why its prognostic significance remains uncertain. In this manuscript, we have focused on risk factors, pathophysiology and management of periprocedural autonomic dysfunction. As there is no standardized approach to the treatment of CAS-D, we present an algorithm for the periprocedural management of patients undergoing CAS. The proposed algorithm was developed based on our procedural experience as well as data from the available literature. The Yale Algorithm was successfully implemented at our institution and we are currently collecting data for short- and long-term safety. © 2014 Wiley Periodicals, Inc.

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Section: The Baroreceptor Reflexmentioning

confidence: 99%

Dysautonomic responses during percutaneous carotid intervention

Bujak

Stilp

Meller

et al. 2014

Cathet Cardio Intervent

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show abstract

“…In the present study, AT1 blockade was not applied to 1K1C animals because of the risk of kidney failure. Previous ultra-short term studies with losartan have not shown an improved baroreflex function in this volume-dependent model of renovascular hypertension (1K1C) [43]. …”

Section: Discussionmentioning

confidence: 90%

Sympathoactivation and rho-kinase-dependent baroreflex function in experimental renovascular hypertension with reduced kidney mass

et al. 2014

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BackgroundDysregulation of the autonomic nervous system is frequent in subjects with cardiovascular disease. The contribution of different forms of renovascular hypertension and the mechanisms contributing to autonomic dysfunction in hypertension are incompletely understood. Here, murine models of renovascular hypertension with preserved (2-kidneys-1 clip, 2K1C) and reduced (1-kidney-1 clip, 1K1C) kidney mass were studied with regard to autonomic nervous system regulation (sympathetic tone: power-spectral analysis of systolic blood pressure; parasympathetic tone: power-spectral analysis of heart rate) and baroreflex sensitivity of heart rate by spontaneous, concomitant changes of systolic blood pressure and pulse interval. Involvement of the renin-angiotensin system and the rho-kinase pathway were determined by application of inhibitors.ResultsC57BL6N mice (6 to 11) with reduced kidney mass (1K1C) or with preserved kidney mass (2K1C) developed a similar degree of hypertension. In comparison to control mice, both models presented with a significantly increased sympathetic tone and lower baroreflex sensitivity of heart rate. However, only 2K1C animals had a lower parasympathetic tone, whereas urinary norepinephrine excretion was reduced in the 1K1C model. Rho kinase inhibition given to a subset of 1K1C and 2K1C animals improved baroreflex sensitivity of heart rate selectively in the 1K1C model. Rho kinase inhibition had no additional effects on autonomic nervous system in either model of renovascular hypertension and did not change the blood pressure. Blockade of AT1 receptors (in 2K1C animals) normalized the sympathetic tone, decreased resting heart rate, improved baroreflex sensitivity of heart rate and parasympathetic tone.ConclusionsRegardless of residual renal mass, blood pressure and sympathetic tone are increased, whereas baroreflex sensitivity is depressed in murine models of renovascular hypertension. Reduced norepinephrine excretion and/or degradation might contribute to sympathoactivation in renovascular hypertension with reduced renal mass (1K1C). Overall, the study helps to direct research to optimize medical therapy of hypertension.

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“…Although GCIP-27could lower blood pressure in spontaneously hypertensive rats, the hypotensive effect of GCIP-27 is significant weaker than that of losartan. And due to compensation, the normotensive animals, such as rats, dogs and patients, are less sensitive to hypotensive agents, such as losartan and nitroprusside, etc., than hypertensive subjects [ 32 , 33 ]. We have also ever observed that GCIP-27 had no influence on the blood pressure in normotensive rats [ 17 , 19 ].…”

Section: Discussionmentioning

confidence: 99%

Gαq Protein Carboxyl Terminus Imitation Polypeptide GCIP-27 Improves Cardiac Function in Chronic Heart Failure Rats

Tong

Liu

et al. 2015

PLoS ONE

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BackgroundGαq protein carboxyl terminus imitation polypeptide (GCIP)-27 has been shown to alleviate pathological cardiomyocyte hypertrophy induced by various factors. Pathological cardiac hypertrophy increases the morbidity and mortality of cardiovascular diseases while it compensates for poor heart function. This study was designed to investigate the effects of GCIP-27 on heart function in rats with heart failure induced by doxorubicin.Methods and ResultsForty-eight rats were randomly divided into the following six groups receiving vehicle (control), doxorubicin (Dox), losartan (6 mg/kg, i.g.) and three doses of GCIP-27 (10, 30, 90 μg/kg; i.p., bid), respectively. Heart failure was induced by Dox, which was administered at a 20 mg/kg cumulative dose. After 10 weeks of treatment, we observed that GCIP-27 (30, 90 μg/kg) significantly increased ejection fraction, fraction shortening, stroke volume and sarcoplasmic reticulum Ca2+ ATPase activity of Dox-treated hearts. Additionally, GCIP-27 decreased myocardial injury, heart weight index and left ventricular weight index, fibrosis and serum cardiac troponin-I concentration in Dox-treated mice. Immunohistochemistry, western blotting and real-time PCR experiments indicated that GCIP-27 (10–90 μg/kg) could markedly upregulate the protein expression of myocardial α-myosin heavy chain (MHC), Bcl-2, protein kinase C (PKC) ε and phosphorylated extracellular signal-regulated kinase (p-ERK) 1/2 as well as the mRNA expression of α-MHC, but downregulated the expression of β-MHC, Bax and PKC βII, and the mRNA expression levels of β-MHC in Dox-treated mice. It was also found that GCIP-27 (30, 90 μg/L) decreased cell size and protein content of cardiomyocytes significantly in vitro by comparison of Dox group.ConclusionsGCIP-27 could effectively ameliorate heart failure development induced by Dox. PKC–ERK1/2 signaling might represent the underlying mechanism of the beneficial effects of GCIP-27.

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Acute AT1 receptor blockade does not improve the depressed baroreflex in rats with chronic renal hypertension

Cited by 5 publications

References 18 publications

Dysautonomic responses during percutaneous carotid intervention

Dysautonomic responses during percutaneous carotid intervention

Sympathoactivation and rho-kinase-dependent baroreflex function in experimental renovascular hypertension with reduced kidney mass

Gαq Protein Carboxyl Terminus Imitation Polypeptide GCIP-27 Improves Cardiac Function in Chronic Heart Failure Rats

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