【高血压英文ppt课件】Hypertension-and-the-Kidney

,*,*,*,Hypertension and the Kidney,Chong Myung Kang,M.D.,Department of Internal Medicine,Hanyang University Hospital,Hypertension and the Kidney,A.The Role of the Kidney in Hypertension,B.Hypertension as a Cause of Renal,Disease,C.Hypertension as a Risk Factor for the,Progression of Renal Disease,D.Hypertension as a Consequence of,Renal Disease,Role of Kidney in Hypertension,1.Pressure-Volume Regulation,2.Congenital Oligonephropathy,3.Renal Transplantation Studies,4.Salt and Hypertension,Fig.2.,Predicted Long-term effects of a peripheral vasoconstrictor that has a relatively week effect on pressure natriuresis.The normal curve(Solid line)is compared with the vasoconstrictor curve(dash line).Initially,the vasoconstrictor would cause natriuresis,because increased peripheral vascular resistance elevates arterial pressure(from point A to point B)above the set-point for balance between intake and output of sodium due to increased.However,increased arterial pressure would cause a transient natriuresis and a reduction in extracellular fluid volume until arterial pressure eventually stabilized at a level(point C)at witch sodium intake and output are balanced.,Fig.3.,Proposed mechanism of pressure natriuresis,Pressure-natriuresis(2),(Medullary Blood Flow),Medullary blood flow(MBF)comprise only 1%of RBF,but important effect on pressure-natriuresis,Endocrine¶crine factors(renal nerve,Ang II prostaglandin,ANP,NO,kinin,vasopressin modulate RPP&urine excretion by regulation of medullary blood flow,Reduce MBF;sympathetic N stimulation,CO inhibition,kinin antagonist,NO synthase inhibition,Ang II,AVP-raise BP,Increase MBF;ANP,prostaglandin,bradykinin,acetylcholine,CEI,Ca blocker-lowering BP,Pressure-natriuresis(3),Abnormal pressure-natriuresis in essential hypertension,1.Increased preglomerular resistance,widespread vasoconstriction of preglomerular,vessels(arteriosclerosis,vasoconstrictors),-relieved with Ca blockers,2.Increased tubular reabsorption,excessive mineralocorticoid,Ang II,(Salt-sensitive;depend on salt intake),Pressure-natriuresis(4),3.Decreased glomerular capillary filtration,coefficient(K,f,),Essential HP with subtle dysfunction in glomerular capillary membrane,glomerulonephritis,4.Reduced number of functioning nephrons,Hyperfiltratioh-glomerulosclerosis,Fig.4.,Steady-state relationships between arterial pressure and urinary sodium ecreation and,sodium intake for normal kidney and four types of renal dysfunction that cause,hypertension:decreased kidney mass,increased reabsorption in distal and collecting,tubules,reduction in glomerular capillary filtration coefficient(K,f,),and increased,preglomerular resistance.,Congenital Oligonephropathy,Low birth weight baby-higher incidence of hypertension in maturity,Fewer nephrons,smaller kidney to body size (Japanese,African-American;adapted to less salt&water in tropical area-HP in salt replete state),Nephron number;genetic,conditions in utero,(300,000-1,000,0000;low socioeconomic state,rat experiment,SHR),Low birth weight,short stature;higher incidence of NIDDM,nephropathy in IDDM,Renal Transplantation Studies,Hypertension can travel with kidney,F1 hybrids(F1H)from WKY,After bilateral nephrectomy,CEI treated SHR&WKY kidney transplanted to F1H,Recipient of SHR-HP,recipient of WKY-normal,No difference between 2 group in BUN,RBF,GFR,Genetic predisposition for HP in donors is required to elicit post-transplantation HP,SHR;decreased capacity to excrete dietary Na,Thus,intrinsic renal mechanism play a major role in manifestation of primary hypertension,Fig.5.,Effects of renal cross-transplantations on systolic blood pressure in five different animal medels of genetic hypertension.,A.,Normotensive recipients received a kidney from hypertensive donors.B.Hypertensive recipients received a kidney from normotensive donors.Symbols are,:(,)Dahl salt-senstive hypertensive rats;()Milan hypetensive rats and Milan normotensive rats;(,)Prague hypertensive rats and Prague normotensive rats;,Normotensive Wistar Kyoto rats(donors),spontaneously hypertensive rats and F1 hybrids(recipients)bred from the first two strains;(,)normotensive Wistar-Kyoto rats(donors),stroke-prone spontaneously hypertensive rats(donors)and F1,hybrids(recipients)bred from the first two strain.,Fig.6.,Blood pressure in human renal graft recipients at one year after transplantation.Based on indirect evidence,donors were assumed to have been normotensive(,)or hypertensive().The differences in blood pressure between recipients of a kidney from normotensive and hypertensive donor occurred despite more vigorous antihypertensive treatment in the latter.,Salt and Hypertension(1),Aberrant response of tubuloglomerular feedback,(TGF)to salt load is responsible for essential HP,Afferent arteriole contract or relax in response to inc.or dec.in macula densa Cl,-,delivery(autoregulation of RBF),Fine tuning of SNGFR through TGF,Low salt intake-dec.afferent arteriolar resistance&TGF,-maintain GPF&Ang II inc.R,E,-maintain P,