1887

Hypertension and the kidney

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Abstract

Systemic arterial hypertension is defined as sustained elevation in blood pressure. This chapters considers pathogenesis of systemic hypertension in patients with kidney disease; impact of systemic hypertension on renal function in kidney disease; treatment strategies for patients with systemic arterial hypertension and kidney disease; and monitoring the patient with systemic hypertension and CKD.

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Figures

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18.2 Relationship between mean arterial pressure and intraglomerular pressure. In the normal kidney (dashed line), renal autoregulation maintains constant glomerular capillary pressure over a relatively wide range of renal arterial ‘input’ pressures. However, in the diseased kidney (solid line), autoregulatory capabilities are impaired, allowing more direct transmission of systemic pressure to the glomerular capillary. As a result, the pressure in the glomerular capillary increases in a more linear fashion over the same range of arterial pressures, increasing the susceptibility to renal injury.
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18.3 Suggested general approach to the treatment of systemic hypertension in dogs and cats with kidney disease. ACEi = angiotensin-converting enzyme inhibitor; IRIS = International Renal Interest Society; SBP = systolic arterial blood pressure; sCr = serum creatinine level; sK = serum potassium level.
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18.4 Effects of changes in renal arteriolar resistance on glomerular capillary pressure and glomerular filtration rate (GFR). Interventions or substances that preferentially constrict the afferent arteriole (AA) (e.g. adenosine) or dilate the efferent arteriole (EA) (e.g. angiotensin-converting enzyme inhibitors) may lead to reductions in glomerular capillary pressure (P) and, therefore, GFR. Conversely, interventions or substances that preferentially constrict the efferent arteriole (e.g. angiotensin II via the AT1 receptor, catecholamines via the beta-1-adrenoreceptor) or dilate the afferent arteriole (e.g. -type calcium channel blockers) lead to increases in P and, therefore, GFR. (Courtesy of the University of Georgia)
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18.6 Overview of the renin–angiotensin–aldosterone system (RAAS) and the site of action of drugs interacting with this system. Renin is released from the juxtaglomerular apparatus in response to a number of physiological stimuli or in certain pathological states. This enzyme cleaves angiotensinogen, produced by the liver, to create the inactive peptide angiotensin I (1). Angiotensin-converting enzyme (ACE) then cleaves angiotensin I to produce the biologically active angiotensin II (2). Angiotensin II is the major effector of the RAAS, and is able to exert its effects by interacting with two receptors, the angiotensin II subtype 1 (AT) receptor, and the angiotensin II subtype 2 (AT2) receptor (3). The AT receptor mediates effects that ultimately result in increased systemic arterial BP, while the AT2 receptor is responsible for beneficial countereffects. Stimulation of AT receptors on the efferent arteriole causes vasoconstriction of this vessel, which increases glomerular capillary pressure and may contribute to the development of glomerular hypertension (4). See text for further details regarding the drugs that interact with this system. ACEi = angiotensin-converting enzyme inhibitor; ARB = angiotensin II type 1 receptor blocker; β1-blocker = beta-1 adrenoreceptor blocking agent. (Courtesy of the University of Georgia)

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