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Page 16

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





Nephrology 2018

Journal of Clinical Nephrology and Therapeutics


Volume 2


International Conference on

Jose Pedro A, J Clin Nephrol Ther 2018, Volume 2



Jose Pedro A

The George Washington University School of Medicine & Health Sciences, USA


rgan 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 (


) or


gene in mice causes salt-sensitive hypertension. Se-

lective silencing of


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


[email protected]