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Role of the Renal Microcirculation in Antihypertensive Therapy

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Role of the Renal Microcirculation in Antihypertensive Therapy REVIEW ICME CREDIT \ Role of the renal microcirculation in antihypertensive therapy SHARON R. 1NMAN, PHD; NICHOLAS T. STOWE, PHD; DONALD G. VIDT, MD BACKGROUND The renal circulation plays a central role in regulating blood pressure and glomerular filtration. YPERTENSION IS OBJECTIVE To examine the effects of the various classes Hcharacterized by an of antihypertensive agents on the renal microcirculation. increase in peripheral vascular resistance, SUMMARY Peripheral vascular resistance is generally increased in generally in proportion to the hypertension, and the microcirculation makes the major contribution elevation in blood pressure. In to resistance. In the kidney, the preglomerular and postglomerular ves- the early stages of hypertension, sels constrict to protect the glomerular capillary from increased hydro- the increase in resistance is lim- static pressure, further increasing peripheral resistance. Because the ited to the kidney; in the later renal microcirculation adjusts to maintain glomerular filtration and stages the increase is shared by blood flow, antihypertensive agents that can normalize the pressure most organ systems.1 This re- and blood flow in these vessels may help prevent the long-term conse- sponse is thought to occur in the quences of hypertension. Angiotensin-Converting enzyme inhibitors resistance vessels 23; the largest, directly affect preglomerular and postglomerular resistance, but they rather than the smallest arteri- further decrease postglomerular resistance. Calcium antagonists selec- oles, make the greatest contribu- tively decrease preglomerular resistance. The diuretics, vasodilators, al- tion to resistance,4 both in hyper- pha blockers, and beta blockers may also cause changes in tension and in normal blood preglomerular and postglomerular resistance; however, compensatory pressure. reflex responses may mitigate their direct effects. The increase in peripheral vas- cular resistance in hypertension CONCLUSION Some antihypertensive agents have unique serves several purposes. It protects actions on the renal microcirculation that better maintain renal structures distal to the resistance function. A basic understanding of the physiologic action of these vessels from excessive hydrostatic agents on the microcirculation may help in their selection. pressure and maintains a normal or slightly elevated pressure in the • INDEX TERMS: ANTIHYPERTENSIVE AGENTS; RENAL CIRCULATION; MICRO- CIRCULATION • CLEVE CLIN J MED 1994; 61:356-362 capillaries to drive the Starling forces necessary for the proper ex- From the Departments of Urology (S.R.I., N.T.S.) and Nephrology change of oxygen, nutrients, and and Hypertension (D.G.V.), The Cleveland Clinic Foundation. metabolic products between the Address reprint requests to S.R.I., Department of Urology, FFB-33, blood and the tissue parenchyma. The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH Adjustments in the renal micro- 44195. circulation also help regulate re- nal blood flow, glomerular filtra- tion, and salt and water excretion 356 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 61 • NUMBER 5 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. RENAL MICROCIRCULATION • INMAN AND ASSOCIATES (Figure). Unfortunately, the increase in resistance tends to drive the systemic blood pressure up further. Later in hypertension, glomerular hydrostatic pres- sure increases and causes glomerular damage, at least 5,6 in various experimental situations. Normal This review focuses on the effect of antihyperten- sive agents on the renal microcirculation, how these effects may contribute to the antihypertensive ac- tion of various drugs, and how antihypertensive Efferent agents that can normalize renal microvascular pres- sure and blood flow may help prevent the long-term consequences of hypertension. EFFECTS OF HYPERTENSION ON THE KIDNEY Hypertension may alter three regulatory mecha- nisms that control the renal microcirculation.' First, there may be morphologic changes within the renal microvasculature, in which hypertrophy of the ves- sel wall reduces the lumen diameter and decreases the ability of the vessel to dilate.8 This results in an increased resistance to flow, further exacerbating the elevated peripheral resistance. FIGURE. Effect of hypertension on glomerular capillary pressure (PKc)- The afferent and efferent vessels normally Second is a change in the kidney's ability to constrict or dilate in response to variations in blood pres- autoregulate in response to alterations in systemic sure to keep the Pgc constant. In early hypertension, Pf.c re- arterial pressure. Renal autoregulation is thought to mains constant, hut later in the disease P^ tends to rise. The glomerular filtration rate is influenced by the PKO the include two components: an intrinsic myogenic hydrostatic pressure within Bowman's capsule, the oncotic component and the tubuloglomerular feedback pressures within the capillary and within the capsule, and mechanism.9 The myogenic response causes the ves- the permeability of the capillary membrane. sels to dilate when perfusion pressure declines and to constrict when perfusion pressure increases. In ex- perimental models of hypertension, this intrinsic compared with normotensive animals.15"17 This may myogenic response is either abolished or reset to a contribute to increased renal vascular resistance. greater pressure.10"12 Tubuloglomerular feedback is the relationship be- ANTIHYPERTENSIVE AGENTS tween the glomerular filtration rate (GFR) and the flow of sodium chloride past the macula densa. Our understanding of the pharmacologic effects When renal perfusion increases, so does the GFR. of antihypertensive agents is based to a certain ex- The increased flow of sodium chloride past the mac- tent on experimental studies and indirect assump- ula densa initiates the tubuloglomerular feedback tions. This section will discuss the major classes of response—an afferent vasoconstriction that returns antihypertensive agents and their proposed mecha- the GFR to normal. In hypertension, tubulo- nisms of action on the renal microcirculation. glomerular feedback is thought to be impaired." Angiotensin II also modulates tubuloglomerular Angiotensin-Converting enzyme inhibitors feedback.14 Because angiotensin II constricts both afferent The third altered mechanism in hypertension is a and efferent arterioles,1^ "20 angiotensin-converting change in vascular responses to vasoactive hor- enzyme (ACE) inhibitors should therefore interfere mones.' Renal vascular responses and the afferent with the effect of angiotensin II at both sites. Data and efferent arteriolar responses to vasoconstrictors from micropuncture experiments substantiate this. such as angiotensin II, norepinephrine, and throm- Anderson et aP confirmed that an ACE inhibitor boxane are exaggerated in hypertensive animals could preserve renal structure and function. They SEPTEMBER • OCTOBER 1994 CLEVELAND CLINIC JOURNAL OF MEDICINE 357 Downloaded from www.ccjm.org on October 1, 2021. For personal use only. All other uses require permission. RENAL MICROCIRCULATION • HUMAN AND ASSOCIATES produced systemic and glomerular hypertension in pendent hypertension.24,25 Selective ATI blockade is rats by performing "5/6 nephrectomies" (removing as effective as ACE inhibition in preventing one whole kidney and two thirds of the other). One glomerulosclerosis in spontaneously hypertensive group was treated with an ACE inhibitor (enalapril), rats with reduced renal mass.26 The role of AT2 and the other group was treated with a combination receptors is less well defined. The AT2 receptors are of reserpine, hydralazine, and hydrochlorothiazide. found in large preglomerular vessels.27 Vasoconstric- Both regimens effectively reduced systemic blood tion in the larger interlobular artery is mediated by pressure; however, the rats treated with enalapril had both ATI and AT2 receptors, but ATI receptors lower glomerular pressures and less proteinuria and have greater influence. The afferent and efferent glomerulosclerosis. This suggests that ACE inhibi- arteriolar responses to angiotensin II are mediated tors dilate both afferent and efferent arterioles; the predominantly by ATI receptors.28 efferent arteriolar dilation reduced the glomerular From these recent findings one can infer that capillary pressure and thus protected against further AT2-receptor antagonists produce their greatest ef- structural damage. fects in the large preglomerular vessels. Because of Efferent arterioles may be more sensitive to the prominent role of ATI receptors in the renal angiotensin II than are interlobular arteries and af- microvasculature, blockade of these receptors will ferent arterioles. Thus, the inhibition of converting- reduce intraglomerular pressure by reversing the enzyme activity may be manifested by a greater de- angiotensin II-induced postglomerular vasocon- crease in efferent than in afferent resistance. striction. Several angiotensin II receptor antago- Although it is difficult to show experimentally that nists provide the opportunity for a more specific ACE inhibitors have a greater effect on the efferent blockade of the renin-angiotensin system at periph- arteriole,21 this is the commonly proposed site of eral receptor sites, thus obviating the adverse effects their action. associated with bradykinin accumulation that occur ACE inhibitors slow the progressive loss of renal with ACE inhibitors. function in hypertensive patients with diabetic nephropathy.
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