Angiotensin-renin system

In some patients with hypertension and in all patients with cardiac failure, the renin-angiotensin system is activated to an undesired degree, burdening the heart. The consequences of diminished ANG II generation by ACE inhibitors are multiple. In patients with hypertension, blood pressure is reduced as a result... 

Bader M, Paul M, Fernandesz-Alfonso M et al (1994) Molecular biology and biochemistry of the renin-angiotensin system, Chap. 11. In Swales ID (ed) Textbook of hypertension. Blackwell Scientific Publications, Oxford, London, Edinburgh, pp 214-232... 

Bader M, Peters J, Baltatu O et al (2001)Tissue renin-angiotensin systems new insights from experimental animal models in hypertension research. J Mol Med 79 76-102... 

Hermann K, Ring J The renin-angiotensin system in patients with repeated anaphylactic reactions during Hymenoptera venom hyposensitization and sting challenge. Int Arch Allergy Immunol 1997 11 251-256. 

Levi and Silver s groups [28] have shown that mast cells are an additional source of renin and constitute a unique extrarenal renin-angiotensin system they found... 

Remuzzi G, Ruggenenti P, Perico N. Chronic renal diseases renopro-tective benefits of renin-angiotensin system inhibition. Ann Intern Med 2002 136 604-615. 

NSAIDs can cause renal insufficiency when administered to patients whose renal function depends on prostaglandins. Patients with chronic renal insufficiency or left ventricular dysfunction, the elderly, and those receiving diuretics or drugs that interfere with the renin-angiotensin system are particularly susceptible. Decreased glomerular filtration also may cause hyperkalemia. NSAIDs rarely cause tubulointerstitial nephropathy and renal papillary necrosis. 

Limited data on occupationally exposed men indicate that the effect of lead on blood pressure may be mediated in part through the renin-angiotensin system, as evidenced by lead-related increases in plasma renin and angiotensin I levels (Campbell et al. 1985) and the kallikrein-kinin system, as indicated by a correlation between renin and kallikrein (Boscolo et al. 1981). Evidence from patients with essential hypertension and renal impairment suggests that excessive lead absorption may be involved in the development of both conditions (Batuman et al. 1983). 

Victery W, Vander AJ, Shulak JM, et al. 1982b. Lead, hypertension, and the renin-angiotensin system in rats. J Clin Med 99 354-362. 

Beige J, Zilch O, Hohenbleicher H, Ringel J, Kunz R, Distler A, Sharma AM. Genetic variants of the renin-angiotensin system and ambulatory blood pressure in essential hypertension. J Hypertens 1997 15 503-508. 

Dudley C, Keavney B, Casadei B, Conway J, Bird R, Ratcliffe P. Prediction of patient responses to antihypertensive drugs using genetic polymorphisms investigation of renin-angiotensin system genes. J Hypertens 1996 14 259-262. 

Van Ampting JMA, Hijmering ML, Beutler JJ, van Etten RE, Koomans HA, Rabelink TJ, Stroes ESG. Vascular effects of ACE inhibition independent of the renin-angiotensin system in hypertensive renovascular disease. Hypertension 2001 37 40-45. 

Hingorani AD, Stevens PA, Hopper R, Dickerson JEC, Brown MJ. Renin-angiotensin system gene polymorphisms influence blood pressure and the response to angiotensin converting enzyme inhibition. J Hypertens 1995 13[pt. II] 1602—1609. 

Ovarian hormones influence fluid intake by interaction with the brain renin-angiotensin system and it has been shown that gonadal steroids affect brain fluid-electrolyte balance by interactions with vasopressin. Both hyperos-molarity and increased intracranial pressure stimulate vasopressin release and intraperitoneal administration of vasopressin antagonists decrease brain volume. 

Regardless of the etiology, fall in blood pressure (BP) is compensated by an increase in sympathetic outflow, activation of the renin-angiotensin system, and other humoral factors that stimulate peripheral vasoconstriction. Compensatory vasoconstriction redistributes blood away from the skin, skeletal muscles, kidneys, and GI tract toward vital organs (e.g., heart, brain) in an attempt to maintain oxygenation, nutrition, and organ function. 

The development of ascites is related to systemic arterial vasodilation that leads to the activation of the baroreceptors in the kidney and an activation of the renin-angiotensin system, with sodium and water retention and vasoconstrictor production. 

Asada Y, Yamazawa T, Hirose K, Takasaka T, lino M 1999 Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system. J Physiol 521 497-505... 

Kurz, S., Hink, U., Nickenig, G., Borthayre, A. B., Harrison, D. G., Munzel, T., Evidence for a causal role for the renin-angiotensin system in nitrate tolerance. Circulation 99 (1999), p. 3181-3187... 

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