RT Book, Section
A1 Hall, John E.
A1 Granger, Joey P.
A1 Jones, Daniel W.
A1 Hall, Michael E.
A2 Fuster, Valentin
A2 Harrington, Robert A.
A2 Narula, Jagat
A2 Eapen, Zubin J.
SR Print(0)
ID 1191186274
T1 PATHOPHYSIOLOGY OF HYPERTENSION
T2 Hurst's The Heart, 14e
YR 2017
FD 2017
PB McGraw-Hill Education
PP New York, NY
SN 9780071843249
LK accessmedicine.mhmedical.com/content.aspx?aid=1191186274
RD 2024/04/20
AB SummaryThis  chapter  discusses  mechanisms  of  physiological  regulation  of  blood  pressure  (BP)  and  pathophysiological  changes  that  lead  to  hypertension.  Long-term  control  of  BP  occurs  via  the  renal-body  fluid  feedback  system,  which  involves  pressure  natriuresis—the  high-BP-induced  increase  in  sodium  and  water  excretion  by  the  kidney  that  leads  to  a  reduction  of  the  BP.  Impaired  pressure  natriuresis  can  result  from  impaired  renal  function,  altered  activation  of  hormones  that  regulate  salt  and  water  excretion  by  the  kidney  (such  as  those  in  the  renin-angiotensin-aldosterone  system),  or  excessive  activation  of  the  sympathetic  nervous  system  (see  accompanying  Hurst's  Central  Illustration).  In  hypertensive  individuals,  increased  BP  is  sustained  by  a  shift  of  pressure  natriuresis  such  that  a  sodium  balance  is  maintained  at  higher  BP;  therefore,  effective  treatment  requires  the  resetting  of  pressure  natriuresis  toward  normal  BP.  This  resetting  can  be  achieved  by  increasing  renal  excretory  capability  (for  example,  by  using  diuretics)  or  by  reducing  antinatriuretic  influences  on  the  kidney  (for  example,  using  inhibitors  of  the  renin-angiotensin-aldosterone  system).