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N o v e m b e r 2 1 - 2 2 , 2 0 1 8 | M a d r i d , S p a i n
OF EXCELLENCE
IN INTERNATIONAL
MEETINGS
YEARS
Nephrology 2018 Journal of Clinical Nephrology and Therapeutics| Volume 2
NEPHROLOGY AND UROLOGY
International Conference on
Jose Pedro A, J Clin Nephrol Ther 2018, Volume 2
GASTRORENAL AXIS IN THE CONTROL OF
BODY SODIUM HOMEOSTASIS
Jose Pedro A
The George Washington University School of Medicine & Health Sciences, USA
Organ to organ communication is important in the maintenance of normal
fluid and electrolyte balance and blood pressure (BP). The gastrointes-
tinal tract and the kidney are major organs involved in this process. Neural
mechanisms and gut hormones mediate the natriuresis of an oral sodium
load. The flow of sodium into the sodium channels of the stomach antrum
activates a sequence of events, leading to G-cell-mediated increase in gastrin
secretion and its release into the circulation. Of all the gut hormones circulat-
ing in the plasma, gastrin is the one that is reabsorbed to the greatest extent
by renal tubules. Gastrin, via its receptor, the cholecystokinin type B receptor
(CCKBR) in the kidney inhibits renal sodium transport. Germline deletion of
gastrin (Gast) or Cckbr gene in mice causes salt-sensitive hypertension. Se-
lective silencing of Gast in the stomach and duodenum in mice impairs their
ability to excrete an oral sodium load and increases BP. Thus, the gastro-renal
axis, mediated by gastrin, can complement pronatriuretic hormones, such as
dopamine, produced by the kidney in response extracellular fluid volume ex-
pansion, to increase sodium excretion after an oral sodium load. However, BP
is not increased in patients who have had gastric bypass. Indeed, the high BP
can be normalized by gastric bypass because of the release of other entero-
kines. Sleeve gastrectomy actually enhances the increase in plasma gastrin
following a mixed meal. By contrast, Roux-en-Y gastric bypass surgery pre-
vents the increase in plasma gastrin following a mixed meal but either type
of bypass surgery increases plasma levels of natriuretic enterokines, such as
glucagon-like peptide-1 (GLP-1). Gastrin, acting on renal CCKBR, GLP-1, act-
ing on its receptor GLP-1R, also in the kidney, and dopamine produced in the
kidney, acting on D1 dopamine receptors interact to negatively regulate renal
sodium transport and keep the BP in the normal range.
Jose Pedro A received his MD degree, magna cum laude,
meritissimus, from the University of Santo Tomas Phil-
ippines, and placed first in the Philippine National Board
Examinations in Medicine and Surgery. He received his
PhD degree in Physiology from Georgetown Universi-
ty, Washington, DC, USA. The primary goal of Jose’s
research is to determine the genetic and pharmacoge-
netic bases of human essential hypertension and the
metabolic syndrome. He has published more than 380
scientific articles in book chapters and journals. Jose has
received several academic and research awards, includ-
ing the 2003 Lewis K. Dahl Memorial Lecture (American
Heart Association), 2007 Ernest H. Starling Distinguished
Lecture (American Physiological Society) and 2015 Ex-
cellence Award for Hypertension Research (American
Heart Association). A key finding of Jose’s research is
the demonstration of the crucial role of gene variants of
GRK4 in the pathogenesis and personalized treatment of
hypertension.
BIOGRAPHY