Hubungan Patofisiologi Hipertensi dan Hipertensi Renal

Akmarawita Kadir


Introduction : Hypertension is a disease with an incidence rate is still high around the world,
most of the causes of hypertension is unknown (essential hypertension / primary
hypertension), a small portion of hypertension caused by diseases acquired (secondary
hypertension). The unknown cause of Hypertension causing complications of diseases that
worsen it, eg kidney disease (renal disease), and can be a disease that actually cause
hypertension becomes more severe (secondary hypertension). Pathophysiology of essential 

hypertension has been a lot of discussed, but the pathophysiology of renal disease which
causes hypertension still needs to be explored, particularly on the relationship between
primary hypertension and secondary hypertension (hypertension, kidney or renal
Kidney disease is a disease that cause hypertension via the mechanism of resistance
increases blood circulation to the kidneys and a decrease in the glomerular capillary
function which resulted in the release of an important substance-substance such as renin,
angiotensinogen, angiotensin I, angiotensin II, angiotensin converting enzyme (ACE)
inhibitors, aldosterone, bradykinin, nitric oxide (NO), which in turn causes increase blood
pressure (hypertension). Hypertension proved to be a feedback mechanism to suppress the
high renin, renin suppression doesn’t mean anything if kidney disease not treated properly,
and even cause permanently hypertension or even getting worse. The purpose of this article
was to determine the pathophysiology of hypertension, renal hypertension in particular, and
how the relationship between hypertension and renal hypertension (secondary).


Pathophysiology; hypertension; renal hypertension; renin; angiotensin; ACE

Full Text:



Sawicka K, Szczyrk M, Jasrzebska I, Prasal M, Zowlak A, Daniluk J, 2011. Hypertention – The silent killer. Journal of Pre-Clinical and Clinical Research, 5 (2) : 43 – 46

Sherwood L, 2013. Human physiology form cells to systems, the blood vessels and blood presure. Eight Edition. Belmont, USA : Thomson Brooks/Cole

Devicaesaria A, 2014. Hipertensi Krisis, Medicinus Vol 27, No. 3

Silbernagl S, Lang F, 2007. Color Atlat of Pathophysiology. Stuttgart, Germany: Georg Thieme Verlag.

American Heart Association, 2014

Hall JE, Granger JP, Hall ME, 2013. The Kidney. Physiology and pathophysiology of Hypertension. 5th Ed. USA: Elsevier Inc.

Kadir A, 2015. Autoregulasi hipertensi, menentukan jenis hipertensi, prosiding Kongres Nasional IAIFI XVI, simposium seminar dan workshop XXIV, Padang

Garovic VD, Textor SC, 2005. Renovascular Hypertension and Ischemic Nephropathy, Nephrology and Hypertension, Mayo Clinic, Circulation AHA, 112:1362-1374

Sayedi N, Koyama M, Mackin CJ, Levi R, 2002. Ischemia Promotes Renin Activation and Angiotensin Formation in Sympathetic Nerve Terminals Isolated from the Human Heart: Contribution to Carrier-Mediated Norepinephrine Release. The Journal Of Pharmacology And Experimental Therapeutics, Vol. 302, No. 2, 302:539–544

Charved YL & Boulange AQ, 2011, Mini Rivew, Role of adipose tissue renin–angiotensin system in metabolic and inflammatory diseases associated with obesity. international Society of Nephrology, Kidney International 79, 162–16

Benigni A, Cassis P, Remuzzi G, 2010. Angiotensin II revisited: new roles in inflammation, immunology and aging, EMBO Molecular Medicine Vol 2, 247-257

Mechanisms™ is a trademark of Core Health Services Inc., registered in the US and Canada., 2012

Vikrant S, Tiwan SC. Essential hypertension – pathogenesis & pathophysiology, 2001. Journal Indian Academy of Clinical Medicine, 2(3): 140-161

Rahardjo P, 2015. Hubungan Hipertensi dengan Penyakit Ginjal. Indonesia Kidney Care Club, .

Palm F, Nordquist L, 2011. Renal oxidative stress, oxygenation, and hypertension. Am J Physiol Regul Integr Comp Physiol 301: R1229–R1241

Haase VH, 2013. Mechanisms of Hypoxia Responses in Renal Tissue. Science in Renal Medicine, J Am Soc Nephrol 24: 537–541

Hong NJ & JL Garvin, 2015. Endogenous flow-induced nitric oxide reduces superoxide-stimulated Na/H exchange activity via PKG in thick ascending limbs.Am. J. Physiol. Renal Physiol. 308:F444-9



  • There are currently no refbacks.

Copyright (c) 2016 Akmarawita Kadir

Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.



Jurnal Ilmiah Kedokteran Wijaya Kusuma 

ISSN: 1978-2071(print); 2580-5967 (online)
Published by the Institute for Research and Community Services (LPPM) of University of Wijaya Kusuma Surabaya.
Surabaya, Indonesia
Creative Commons License
All publications by Jurnal Ilmiah Kedokteran Wijaya Kusuma are licensed under a Creative Commons Attribution-NonCommercial 4.0 International License
counter View My Stats