Interactions of Renal Prostaglandins, Renin-Angiotensin System and Renal Kallikrein-Kinin System in Human Hypertension

1987 ◽  
pp. 215-220
Author(s):  
K. Abe ◽  
K. Tsunoda ◽  
M. Sato ◽  
K. Omata ◽  
M. Vasujima ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Kinin System ◽  
Angiotensin System ◽  
Human Hypertension ◽  
Renin Angiotensin ◽  
Renal Prostaglandins ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System

Renin-angiotensin system modulates renal bradykinin production

1996 ◽  
Vol 271 (4) ◽  
pp. R1090-R1095 ◽  
Author(s):  
H. M. Siragy ◽  
A. A. Jaffa ◽  
H. S. Margolius ◽  
R. M. Carey
Keyword(s):  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Sodium Depletion ◽  
Kinin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Kallikrein ◽  
Kallikrein Kinin System ◽  
Cgmp Formation

Previous studies have shown that sodium depletion is associated with an increase in renal kallikrein-kinin system activity. This system may play an important role in counterbalancing the renal effects of the renin-angiotensin system. In this study, we examined whether the renal renin-angiotensin system participates in the regulation of renal bradykinin (BK) levels during sodium depletion. We measured changes in renal excretory and hemodynamic function, renal interstitial fluid (RIF) BK, and RIF and urinary guanosine 3',5'-cyclic monophosphate (cGMP) and prostaglandin E2 (PGE2) in conscious uninephrectomized dogs (n = 5) in sodium metabolic balance (10 meq/day) in response to intrarenal arterial administration of the renin inhibitor ACRIP (0.2 microgram.kg-1.min-1) or angiotensin II AT1-receptor blocker losartan (100 ng.kg-1.min-1). ACRIP and losartan increased urine flow rate from 0.75 +/- 0.06 to 1.6 +/- 0.03 and 1.5 +/- 0.05 ml/min, respectively (each P < 0.001), and urine sodium excretion from 5.4 +/- 0.7 to 18.3 +/- 1.3 and 15.9 +/- 1.2 meq/min, respectively (each P < 0.001). Glomerular filtration rate and renal plasma flow increased only during losartan administration (P < 0.05). ACRIP decreased RIF BK by 48%, from 33.1 +/- 3.8 to 17.4 +/- 4.1 pg/min (P < 0.01). ACRIP decreased RIF cGMP by 38%, from 0.69 +/- 0.08 to 0.43 +/- 0.1 pmol/min (P < 0.01); urinary cGMP by 16%, from 0.63 +/- 0.05 to 0.53 +/- 0.02 pmol/min (P < 0.05); and RIF PGE2 by 46%, from 10.5 +/- 1.1 to 5.7 +/- 1.1 pg/min (P < 0.01). Urinary PGE2 was unchanged by ACRIP. Losartan decreased RIF PGE2 by 71%, from 10.8 +/- 0.6 to 3.1 +/- 0.6 pg/min (P < 0.01) but failed to change RIF BK, RIF cGMP, urinary cGMP, or urinary PGE2. These data suggest that the renin-angiotensin system tonically stimulates renal BK production and cGMP formation via a non-AT1 angiotensin receptor and renal PGE2 production via the AT1 receptor.

scholarly journals Differences in the expression of the renin angiotensin system and the kallikrein-kinin system during the course of myocardial infarction in male and female Wistar rats

2020 ◽  
Vol 21 (2) ◽  
pp. 147032031990003
Author(s):  
Jazmín Flores-Monroy ◽  
Diego Lezama-Martínez ◽  
Salvador Fonseca-Coronado ◽  
Luisa Martínez-Aguilar
Keyword(s):  
Myocardial Infarction ◽  
Angiotensin Converting Enzyme ◽  
Wistar Rats ◽  
Renin Angiotensin System ◽  
Converting Enzyme ◽  
Kinin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Female Wistar Rats ◽  
Kallikrein Kinin System

Background: There is some evidence that components of the renin-angiotensin system and kallikrein-kinin system are not similarly regulated in both sexes. The aim of this work was to analyze the expression of angiotensin-converting enzyme, angiotensin-converting enzyme 2, angiotensin 1 receptor, angiotensin 2 receptor, beta-1 receptor, and beta-2 receptor during the evolution of myocardial infarction. Methods: Thirty-six male and 36 female Wistar rats were used. Myocardial infarction was induced. Six groups of both sexes were formed, ( n=6): (a) sham; (b) 48 h myocardial infarction; (c) one week myocardial infarction; (d) two weeks myocardial infarction; (e) three weeks myocardial infarction and (f) four weeks myocardial infarction. The expression was evaluated by real-time polymerase chain reaction on the penumbra of left ventricle. Results: The mRNA expression of most biomarkers was lower in females than in males. During acute infarction, an increase of all protein expression was found in female and at two weeks while in the male only biomarker changes occurred at three weeks. In addition, in male biomarkers mRNA expression decreased during chronic infarction while in females it did not. Conclusions: The renin-angiotensin system and kallikrein-kinin system biomarkers expression occurs at earlier times in the female than in the male rat. In addition, during chronic myocardial infarction these biomarkers remained unchanged in females while in males they decreased.

scholarly journals The renin-angiotensin system and its blockers

2014 ◽  
Vol 142 (11-12) ◽  
pp. 756-763 ◽  
Author(s):  
Rajko Igic ◽  
Ranko Skrbic
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Biologically Active ◽  
Kinin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Active Peptides ◽  
History Of ◽  
Essential Connection ◽  
Kallikrein Kinin System

Research on the renin-angiotensin system (RAS) has contributed significantly to advances in understanding cardiovascular and renal homeostasis and to the treatment of cardiovascular diseases. This review offers a brief history of the RAS with an overview of its major components and their functions, as well as blockers of the RAS, their clinical usage and current research that targets various components of the RAS. Because angiotensin-converting enzyme (ACE) metabolizes two biologically active peptides, one in the kallikrein-kinin system (KKS) and one in the RAS, it is the essential connection between the two systems. ACE releases very powerful hypertensive agent, angiotensin II and also inactivates strong hypotensive peptide, bradykinin. Inhibition of ACE thus has a dual effect, resulting in decreased angiotensin II and increased bradykinin. We described the KKS as well.

scholarly journals Kallikrein–kinin system as the dominant mechanism to counteract hyperactive renin–angiotensin system

2017 ◽  
Vol 95 (10) ◽  
pp. 1117-1124 ◽  
Author(s):  
Domenico Regoli ◽  
Fernand Gobeil
Keyword(s):  
Renin Angiotensin System ◽  
Biologically Active ◽  
Ang Ii ◽  
Kinin System ◽  
Angiotensin System ◽  
Dominant Mechanism ◽  
Renin Angiotensin ◽  
First Choice ◽  
Kallikrein Kinin System ◽  
The Impact

The renin–angiotensin system (RAS) generates, maintains, and makes worse hypertension and cardiovascular diseases (CVDs) through its biologically active component angiotensin II (Ang II), that causes vasoconstriction, sodium retention, and structural alterations of the heart and the arteries. A few endogenous vasodilators, kinins, natriuretic peptides, and possibly angiotensin (1-7), exert opposite actions and may provide useful therapeutic agents. As endothelial autacoids, the kinins are potent vasodilators, active natriuretics, and protectors of the endothelium. Indeed, the kallikrein–kinin system (KKS) is considered the dominant mechanism for counteracting the detrimental effects of the hyperactive RAS. The 2 systems, RAS and KKS, are controlled by the angiotensin-converting enzyme (ACE) that generates Ang II and inactivates the kinins. Inhibitors of ACE can reduce the impact of Ang II and potentiate the kinins, thus contributing to restore the cardiovascular homeostasis. In the last 20 years, ACE-inhibitors (ACE-Is) have become the drugs of first choice for the treatments of the major CVDs. ACE-Is not only reduce blood pressure, as sartans also do, but by protecting and potentiating the kinins, they can reduce morbidity and mortality and improve the quality of life for patients with CVDs. This paper provides a brief review of the literature on this topic.

The kallikrein-kinin and the renin-angiotensin systems have a multilayered interaction

2003 ◽  
Vol 285 (1) ◽  
pp. R1-R13 ◽  
Author(s):  
Alvin H. Schmaier
Keyword(s):  
Cross Talk ◽  
Physiological Role ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Kinin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Two Systems ◽  
Kallikrein Kinin System

Understanding the physiological role of the plasma kallikrein-kinin system (KKS) has been hampered by not knowing how the proteins of this proteolytic system, when assembled in the intravascular compartment, become activated under physiological conditions. Recent studies indicate that the enzyme prolylcarboxypeptidase, an ANG II inactivating enzyme, is a prekallikrein activator. The ability of prolylcarboxypeptidase to act in the KKS and the renin-angiotensin system (RAS) indicates a novel interaction between these two systems. This interaction, along with the roles of angiotensin converting enzyme, cross talk between bradykinin and angiotensin-( 1 – 7 ) action, and the opposite effects of activation of the ANG II receptors 1 and 2 support a hypothesis that the plasma KKS counterbalances the RAS. This review examines the interaction and cross talk between these two protein systems. This analysis suggests that there is a multilayered interaction between these two systems that are important for a wide array of physiological functions.

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