Endothelin Antagonism Does Not Affect Adrenal Catecholamine Secretion and System Haemodynamics During Acute Stress in Wistar Rats

Zaretsky, Dmitry V.; Zaretskaia, Maria V.; Kalenikova, E. I.; Grafov, Mikhail A.

doi:10.1097/00005344-200036051-00108

Cited by 3 publications

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“…Zaretskyl et al (868) studied the effect of restraint stress on ET-induced adrenal catecholamine release in conscious male Wistar rats chronically instrumented with vascular catheters and a microdialysis probe placed into the adrenal gland. Norepinephrine and epinephrine levels in adrenal perfusate were stable at baseline and increased significantly with restraint stress, associated with concomitant elevation in BP and heart rate.…”

Section: Endothelin and Humoral Systemsmentioning

confidence: 99%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

367

459

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Endothelin (ET) peptides and their receptors are intimately involved in the physiological control of systemic blood pressure and body Na homeostasis, exerting these effects through alterations in a host of circulating and local factors. Hormonal systems affected by ET include natriuretic peptides, aldosterone, catecholamines, and angiotensin. ET also directly regulates cardiac output, central and peripheral nervous system activity, renal Na and water excretion, systemic vascular resistance, and venous capacitance. ET regulation of these systems is often complex, sometimes involving opposing actions depending on which receptor isoform is activated, which cells are affected, and what other prevailing factors exist. A detailed understanding of this system is important; disordered regulation of the ET system is strongly associated with hypertension and dysregulated extracellular fluid volume homeostasis. In addition, ET receptor antagonists are being increasingly used for the treatment of a variety of diseases; while demonstrating benefit, these agents also have adverse effects on fluid retention that may substantially limit their clinical utility. This review provides a detailed analysis of how the ET system is involved in the control of blood pressure and Na homeostasis, focusing primarily on physiological regulation with some discussion of the role of the ET system in hypertension.

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Section: Endothelin and Humoral Systemsmentioning

confidence: 99%

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Kohan

Rossi

Inscho

et al. 2011

Physiological Reviews

367

459

View full text Add to dashboard Cite

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“…The stress of immobilization causes a marked and sustained increase in heart rate, mean arterial pressure, and catecholamine secretion in rats [49]. White-coat hypertension has been described in patients who have elevated blood pressure in the doctor's office but normal values during 24-hr ambulatory recordings [7,47].…”

Section: Discussionmentioning

confidence: 99%

Heart Rate Modulation by Sympathetic Nerves in Dogs with Heart Failure.

Uechi

Shimizu

Mizuno

2002

The Journal of Veterinary Medical Science

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ABSTRACT. To clarify heart rate modulation by the sympathetic nervous system, dogs with naturally acquired and experimentally induced heart failure were examined. Heart rate and plasma catecholamine concentrations were measured in clinically healthy dogs (contr ol dogs) and dogs with mitral regurgitation (MR) during a resting period, a standing period, a period of standing in a medical examination room (to which the dogs were unaccustomed), a running period, and a period of recovery after running. The heart rate and plasma cate cholamine concentration increased in control dogs during the standing period and the medical examination room period, relative to the resting period. However, dogs with MR did not exhibit any clear increase in heart rate or catecholamine concentration under these light stress conditions. Running stress increased plasma catecholamine levels in control dogs; however, dogs with MR did not exhibit any significant changes. Thirty-two dogs with naturally acquired heart disease were classified as grades I to III on the ISACHC scale. The degree of increase in heart rate and plasma catecholamine levels in dogs with naturally acquired heart failure depended on their degree of heart failure. In conclusion, an increased heart rate and an activated sympathetic nervous system were observed, even in mild heart failure. This chronically activated sympathetic activity is expected to increase myocardial oxygen consumption, myocardial hypertrophy, and fibrosis, and to portend a poorer prognosis in heart failure. KEY WORDS: catecholamine, exercise, mitral regurgitation, stress.J. Vet. Med. Sci. 64(11): 1023-1029, 2002 Congestive heart failure (CHF) is characterized by increased peripheral vascular resistance and tachycardia. The reduced cardiac output in cardiac disease leads to failure of the peripheral blood circulation because of decreased parasympathetic tone and increased sympathetic tone [1,9,32,36,38,39]. Neurohumoral activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis, etc. increases circulating blood volume and arterial pressure by causing vasoconstriction and sodium and fluid retention [16]. Elevated plasma noradrenaline (NA) has been shown to contribute to the pathological chronotropic response, which leads to progression of CHF [9,32,36,38,39,44]. Chronic adrenergic stimulation has been shown to have a direct cardiotoxic effect [22,26], and elevated NA levels are associated with a poorer prognosis and increased mortality [9,11,31].The purpose of this study was to measure the plasma concentrations of the catecholamines NA and adrenaline (AD) in dogs with naturally acquired heart disease, mitral regurgitation (MR), tricuspid regurgitation (TR), and dilated cardiomyopathy and right ventricle heart failure due to Dirofilalia imitis infection. We also evaluated in changes in the plasma concentrations of NA and AD during rest, light stress, running, and recovery from running in iatrogenic mitral regurgitation dogs. MATERIALS AND METHODSThe methods used in this study ...

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Endothelin-Converting Enzyme Inhibition in the Rat Model of Acute Heart Failure: Heart Function and Neurohormonal Activation

Rufanova

Pozdnev²,

Kalenikova³

et al. 2009

Exp Biol Med (Maywood)

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Endothelin-1 (ET-1) has been implicated in many cardiovascular diseases, including acute heart failure (AHF) due to myocardial ischemia. Previously we described the oral endothelin-converting enzyme (ECE) inhibitor, PP36, and in this study, we investigated its cardioprotective effect in more detail, and examined the role of PP36 in the neurohormonal activation in rats that had been subjected to acute myocardial ischemia due to the microsphere embolization of coronary microcirculation. PP36 treatment (3.5 x 10(-5) M/kg/day) led to a significant fourfold decrease in hypertensive response when big-ET-1 was administered to healthy, conscious rats. ECE inhibition did not affect mortality during the first 48 hours after ischemia initiation. Systemic hemodynamic, heart function, and neurohormonal activation were analyzed in the healthy control group, the AHF group, and the AHF+PP36 group two days after AHF induction. In conscious rats in the AHF+PP36 group, mean arterial pressure (MAP) was restored and became similar to that of the MAP of the control group. In anesthetized rats, in the AHF+PP36 group, MAP was not restored and was 22% lower than the MAP of the control group. Myocardial contractility was partially restored and cardiac relaxation significantly improved after PP36 application. Further analysis of cardiac output and peripheral resistance in anesthetized rats revealed no differences between the AHF group and the AHF+PP36 group. There were no differences in plasma ET-1 concentration, serum angiotensin converting enzyme activity, and in the adrenal glands' catecholamine content between the AHF group and the AHF+PP36 group. However, rats in the AHF+PP36 group demonstrated a 60% decrease in cardiac endothelial nitric oxide synthase (eNOS) protein expression, and a 56% reduction of myocardial norepinephrine release, when compared with the AHF group's animals. These results suggest that PP36 can preserve heart function during the recovery from acute ischemic injury, and may modulate the cardiac norepinephrine release and eNOS protein level.

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Endothelin Antagonism Does Not Affect Adrenal Catecholamine Secretion and System Haemodynamics During Acute Stress in Wistar Rats

Cited by 3 publications

References 0 publications

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Regulation of Blood Pressure and Salt Homeostasis by Endothelin

Heart Rate Modulation by Sympathetic Nerves in Dogs with Heart Failure.

Endothelin-Converting Enzyme Inhibition in the Rat Model of Acute Heart Failure: Heart Function and Neurohormonal Activation

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