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Wednesday, July 22, 2020 | History

5 edition of Role of Endogenous Epinephrine in the Development of Experimental Hypertension found in the catalog.

Role of Endogenous Epinephrine in the Development of Experimental Hypertension

by O. S. Medvedev

  • 37 Want to read
  • 1 Currently reading

Published by Routledge .
Written in English

    Subjects:
  • Cardiovascular medicine,
  • Medical / Nursing,
  • Medical,
  • Laboratory Medicine,
  • Medical / Laboratory Medicine

  • Edition Notes

    SeriesSoviet Medical Reviews Series, Section a
    The Physical Object
    FormatPaperback
    Number of Pages128
    ID Numbers
    Open LibraryOL9547865M
    ISBN 10371865234X
    ISBN 109783718652341
    OCLC/WorldCa230941911

    1. Introduction. The sympathoadrenal system consisting of sympathetic postganglionic neurons and adrenal medullary chromafin cells release the catecholamines epinephrine, norepinephrine, and dopamine into the blood stream upon activation of the neuronal nicotinic receptors by acetylcholine in preparation for the ‘fight or flight’ reactions. 1–4 The predominant catecholamine released from. Epinephrine is one of two catecholamines released by the activation of the sympathetic nervous system. The other is norepinephrine. Epinephrine prepares the body for quick action. Blood flow shifts from the skin and digestive tract to the muscles, your heart rate increases, your blood pressure rises and you become more alert.

    Epinephrine, hormone secreted mainly by the medulla of the adrenal glands that functions primarily to increase cardiac output and raise blood glucose levels. Epinephrine is released during acute stress and is associated with the fight-or-flight response. Learn more about epinephrine’s production and effects. Epinephrine is a catecholamine, a sympathomimetic monoamine derived from the amino acids phenylalanine and is the active sympathomimetic hormone secreted from the adrenal medulla in most species. It stimulates both the alpha- and beta- adrenergic systems, causes systemic vasoconstriction and gastrointestinal relaxation, stimulates the heart, and dilates bronchi and cerebral .

      Air pollution is the most important environmental risk factor for disease and premature death, and exposure to combustion particles from vehicles is a major contributor. Human epidemiological studies combined with experimental studies strongly suggest that exposure to combustion particles may enhance the risk of cardiovascular disease (CVD), including atherosclerosis, hypertension, . Numerous studies over the last two decades have suggested a central role for oxidative stress in the development of several cardiovascular diseases. This chapter aims to summarize the current experimental and clinical evidence about the major oxidant and antioxidant changes occurring in hypertension and heart failure, and to provide a critical.


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Role of Endogenous Epinephrine in the Development of Experimental Hypertension by O. S. Medvedev Download PDF EPUB FB2

Epinephrine and the Genesis of Hypertension John S. Floras Several lines of evidence suggest a psychophysiological link between stress, adrenomedullary activation, and the genesis of hypertension.

Experimental data support four important concepts: 1) epinephrine stimulates prejunctional ft-adrenergic receptors that facilitate. The hypothesis that intermittent surges in epinephrine could initiate or promote the development of primary hypertension by amplifying peripheral neurotransmission, both directly (facilitative effect) and indirectly (cotransmitter action), is supported by reports that hemodynamic and noradrenergic responses to sympathetic activation can be Cited by: Several lines of evidence suggest a psychophysiological link between stress, adrenomedullary activation, and the genesis of hypertension.

Experimental data support four important concepts: 1) epinephrine stimulates prejunctional beta 2-adrenergic receptors that facilitate norepinephrine release from sympathetic nerve endings; 2) epinephrine can be converted into a cotransmitter by neuronal Cited by:   Role of norepinephrine and epinephrine in development of cardiac hypertrophy.

Early studies by Simpson showed that cultured neonatal rat cardiomyocytes respond to norepinephrine stimulation, with an increase in myocyte size. Furthermore, long-term infusion of catecholamines in experimental animals can induce cardiac by: Epinephrine is a hormone released from the adrenal medulla in response to stress, mediated by sympathetic fibers.

The word epinephrine derives from epi, meaning above, and nephros, the root word for kidney, because the gland sits atop the hrine is also called adrenaline, derived from the name of its this reason, receptors for both epinephrine and norepinephrine are.

This study was performed to investigate the role of endogenous epinephrine in the regulation of vascular tone in hypertension. The release of endogenous epinephrine and norepinephrine from the vascular adrenergic neurons by periarterial nerve stimulation was examined in spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto rats (WKY).

EXPERIMENTAL STUDIES Important Role of Endogenous Norepinephrine and Epinephrine in the Development of In Vivo Pressure-Overload Cardiac Hypertrophy Antonio Rapacciuolo, MD,* Giovanni Esposito, MD,* Kathleen Caron, PHD,† Lan Mao, MD,* Steven A.

The role of endogenous epinephrine in the development of experimental hypertension, O.S. Medvedev and A.I. Kuzmin; use of human atherosclerotic cells for the development of anti-atherosclerotic drugs, A.N. Orekhov; regional peculiarities of vascular effects of opiod peptides and endothelin in experiments on conscious rats, O.S.

Medvedev et al; cyclic nucleotides and. The concomitant reduction of plasma insulin by taurine may suggest the role of hyperinsulinemia in development of hypertension in this model.

A more recent report showed that the prevention of the development of hypertension by taurine (2% in drinking water for 3 weeks) in the FHR was augmented by exercise [ 42 ]. Bertel O, Bühler FR, Kiowski W, Liitold BE: Decreased beta-adrenoceptor responsiveness as related to age, blood pressure, and plasma catecholamines in patients with essential hypertension.

Hypertension 2: –, PubMed Google Scholar. Although there was no effect on the endogenous catecholamines stored in the heart and brain in the diabetic rats, there was a marked increase in the urinary excretion of norepinephrine (NE), epinephrine (E), 3-methoxy-4 hydroxy mandelic acid (VMA) and creatinine.

Abstract. It has long been recognized that opiates may exert potent actions on the cardiovascular system (HOLADAY ). Identification of endogenous opioid peptides and opioid receptors within the central nervous system, particularly at sites associated with central cardiovascular regulation, has led to an examination of their potential role in cardiovascular control both under normal.

46 Rapacciuolo, A. et al. () Important role of endogenous norepinephrine and epinephrine in the development of in vivo pressure-overload cardiac hypertrophy. Journal of the American College of Cardiol Epinephrine and norepinephrine sound alike, and they also share many of the same functions.

Learn more about these two hormones and neurotransmitters, including the differences between them. Role of sympathetic nervous system in experimental hypertension and diabetes mellitus.

India. An investigation has been made to elucidate the role of sympathetic nervous system (SNS) in the development of renal hypertension and hyperglycemia in rats and rhesus monkeys using 6-hydroxydopamine (6-OHDA). Although there was no effect on the. Abstract.

The etiology of hypertension remains unknown, but one fact is clearly established: no single cause is responsible. High blood pressure (BP) is the end result of a number of factors, both genetic and environmental, that may be quantitatively and qualitatively different in different individuals.

Estrogen deficiency is one of the main causes of age-associated diseases in the cardiovascular system. Female Wistar rats were divided into four experimental groups: pharmacologically ovariectomized, surgically ovariectomized, and month-old intact aging animals were compared with a control group.

The activity and expression of heme oxygenases (HO) in the cardiac left ventricle, the. Joey P. Granger, John E. Hall, in Comprehensive Hypertension, An interesting fact to consider is that almost all forms of experimental hypertension are caused by obvious insults to the kidneys that alter renal hemodynamics or tubular reabsorption.

For example, constriction of the renal arteries (e.g., Goldblatt hypertension), compression of the kidneys (e.g., perinephritic hypertension. The endogenous catecholamines adrenaline (epinephrine) and NE [noradrenaline (norepinephrine)] mediate sympathetic regulation of BP (blood pressure).

These effectors of the sympathetic nervous system are synthesized within sympathetic neurons and chromaffin cells of the adrenal medulla by the well-defined series of reactions shown in Figure 1. Epinephrine, more commonly known as adrenaline, is a hormone secreted by the medulla of the adrenal glands.

Strong emotions such as fear or anger cause epinephrine to be released into the bloodstream, which causes an increase in heart rate, muscle strength, blood pressure, and sugar metabolism.

development of this form of hypertension and the role of sodium intake in the pro-ductio n of this abnormality i norepinephrine storage. The productio n of hypertensio i animals treated with DOCA and NaCl is associated with sodium retention. Further-more, the sodium and potassium contents of vascular tissues are increased in this form.Whether and to what extent the sympathetic nervous system participates in the development of essential hypertension has remained largely unclear.

The role of the adrenergic effector — cardiovascular response axis in the pathogenesis of essential hypertension was investigated by combined analysis of blood levels, total plasma clearance and cardiovascular pressor effects of. EO take part in the development of hypertension through increased sympathetic tone, and in direct prohypertrophic effects on myocytes of heart and arteries, as well as causing collagen.