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Books on the topic 'Angiotensins Physiological effect'

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Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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1

Timmermans, P. B. M. W. M. and Wexler Ruth R, eds. Medicinal chemistry of the renin-angiotensin system. Lausanne: Elsevier, 1994.

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2

International Symposium on Cellular and Molecular Biology of the Adrenal Cortex (5th 1992 Avignon, France). Cellular and molelcular biology of the adrenal cortex: Proceedings of the 5th International Symposium on Cellular and Molecular Biology of the Adrenal Cortex held in Avignon (France) August 27-29, 1992. Paris, France: INSERM, 1992.

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3

Ding, Lili. The roles of ERK1/2 and PI3K in abnormal vascular functions in angiotensin II-infused hypertensive rats. St. Catharines, Ont: Brock University, Faculty of Applied Health Science, 2005.

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4

Ahsan, Husain, Graham Robert M, and Victor Chang Cardiac Research Institute., eds. Drugs, enzymes, and receptors of the renin-angiotensin system: Celebrating a century of discovery. Amsterdam: Harwood Academic Publishers, 2000.

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5

Peters, Timothy Francis. Physiological effects of chronic exercise-training and hemorrhage in response to central angiotensin II administration in male rats. 1993.

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6

Flynn, Angela Joanne. Androgenic effects on angiotensin II-induced blood pressure and cochlear blood flow changes in rats. 1990.

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7

Roberts, Kim Alexandria. Anatomical mapping of angiotensin pathways in the central nervous system. 1993.

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8

King, Steven Jay. Effects of angiotensin on central and peripheral tissues involved in blood pressure homeostasis. 1986.

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9

Batt, Carol Mohr. Use of peptidases and peptidase inhibitors to manipulate endogenous levels of angiotensin in normotensive and hypertensive rats. 1992.

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10

Ferrario, Carlos M., Mustafa F. Lokhandwala, and Joseph P. Buckley. Central Actions of Angiotensin and Related Hormones. Elsevier Science & Technology Books, 2013.

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11

Cook, Victoria Irene. Comparison of perinatal angiotensin binding in the brains of SHR and WKY rats. 1991.

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12

W, Harding Joseph, ed. Angiotensin and blood pressure regulation. San Diego: Academic Press, 1988.

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13

Cellular and Molecular Biology of the Adrenal Cortex (Colloques INSERM). J. Libbey Eurotext, 1996.

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14

(Editor), J. M. Saez, and et al (Editor), eds. Cellular and Molecular Biology of the Adrenal Cortex (Colloques Inserm). John Libbey & Co Ltd, 1992.

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15

D, Giles Thomas, ed. Angiotensin-converting enzyme (ACE): Clinical and experimental insights. Fort Lee, N.J: Health Care Communications, Inc., 2001.

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16

Ding, Lili. The roles of ERK1/2 and PI3K in abnormal vascular functions in angiotensin II-infused hypertensive rats. 2005.

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17

Husain, Ahsan, and Robert M. Graham. Drugs, Enzymes and Receptors of the Renin-Angiotensin System: Celebrating a Century of Discovery. Taylor & Francis Group, 2003.

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18

Husain, Ahsan, and Robert M. Graham. Drugs, Enzymes and Receptors of the Renin-Angiotensin System: Celebrating a Century of Discovery. Taylor & Francis Group, 2003.

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19

Husain, Ahsan, and Robert M. Graham. Drugs, Enzymes and Receptors of the Renin-Angiotensin System: Celebrating a Century of Discovery. Taylor & Francis Group, 2000.

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20

Graham, Robert M., and Ahsan Husain. Drugs, Enzymes and Receptors of the Renin-Angiotensin System: Celebrating a Century of Discovery (The Victor Chang Molecular Cardiology Series, V. 1). CRC, 2000.

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21

Dussaule, Jean-Claude, Martin Flamant, and Christos Chatziantoniou. Function of the normal glomerulus. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0044_update_001.

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Abstract:
Glomerular filtration, the first step leading to the formation of primitive urine, is a passive phenomenon. The composition of this primitive urine is the consequence of the ultrafiltration of plasma depending on renal blood flow, on hydrostatic pressure of glomerular capillary, and on glomerular coefficient of ultrafiltration. Glomerular filtration rate (GFR) can be precisely measured by the calculation of the clearance of freely filtrated exogenous substances that are neither metabolized nor reabsorbed nor secreted by tubules: its mean value is 125 mL/min/1.73 m² in men and 110 mL/min/1.73 m² in women, which represents 20% of renal blood flow. In clinical practice, estimates of GFR are obtained by the measurement of creatininaemia followed by the application of various equations (MDRD or CKD-EPI) and more recently by the measurement of plasmatic C-cystatin. Under physiological conditions, GFR is a stable parameter that is regulated by the intrinsic vascular and tubular autoregulation, by the balance between paracrine and endocrine agents acting as vasoconstrictors and vasodilators, and by the effects of renal sympathetic nerves. The mechanisms controlling GFR regulation are complex. This is due to the variety of vasoactive agents and their targets, and multiple interactions between them. Nevertheless, the relative stability of GFR during important variations of systemic haemodynamics and volaemia is due to three major operating mechanisms: autoregulation of the afferent arteriolar resistance, local synthesis and action of angiotensin II, and the sensitivity of renal resistance vessels to respond to NO release.
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