Hypertension affects 20% to 25% of adult population. Most patients are diagnosed as havingessential or primary hypertension. Up to 10% to 15 % have an identifiable cause and many ofthose have an adrenal basis [Miroslava H. et al., 2002]. The tissue kallikrein-kinin (KKS)and renin-angiotension-aldosterone system (RAAS) had been implicated in regulating bloodpressure and electrolyte homeostasis. Recent studies in humans indicate that the vasodilatortissue KKS, the counterpart of the tissue RAAS, is also expressed in the adrenal gland. Theadrenal gland regulates sodium and water excretion and reabsorption through the release ofaldosterone and corticosterone. Previous study reveals an anatomical linkage between thetissue KKS and sodium and water metabolism. Both of the KKS and RAAS may work coordinately toregulate salt metabolism, local blood flow. In contrast, although many investigators havesupported the notion that Ang II and BK physiologically antagonize each other’s effects onblood pressure, there are many instances where the two peptides exert common actions. Forexample, the Bradykinin also stimulates aldosterone release from adrenocortical cells throughB2 receptors. Furthermore, the AT1 receptor and the bradykinin (B2) receptor form stableheterodimers, the two major signaling proteins triggered by AT1. In vitro studies (Margolius1995) have shown that kallikrein acts as a prorenin-activating enzyme, and that tissuekallikrein can generate angiotensin II.However, the interactions between both systems are complex and not always simplyantagonistic. The interactions of the two systems on aldosterone secretion are not examinedThus, we conducted this study to elucidate, first, whether some alterations in components ofthe kallikrein-kinin system could do effect on aldosterone secretion.Our study provides evidence that bradykinin contributes substantially to the aldosteronesecretion with or without the effects of angiotensin. The data also could confirm whetherATR2-Bradykinin-B2-aldosterone really works. We want to realize the expression of angiotensinand bradykinin in the adrenal gland and hypertension related to these systems.Previous study has showed the post captopril plasma aldosterone concentration (PAC)/ plasmarennin activity (PRA) ration (ARR) was a reliable method for diagnosis of primaryaldosteronism (PA). The ARR change by angiotensin II receptor blockade was reported to besignificantly higher than that by ACE inhibitor. This study assessed whether angiotensin IIreceptor blockade offers any additional advantage in the diagnosis of PA. Clinically weevaluated the sensitivity and specificity of captopril (angiotensin-converting enzymeinhibition) and losartan (angiotensin II type 1 receptor blocker) test in PA patient. Thisinteraction mechanism, in term, could further explain the interaction of KKS and RAAS.

Study Name: Kallikrein-kinin (KKS) and Renin-angiotensin-aldosterone System (RAAS) in Primary Aldosteronism
Status: Completed
Conditions: Primary aldosteronism
Interventions: Drug: captopril, Losartan (drug)
Locations: National Taiwan University Hospital, Taipei, Taiwan
Study link:

To search for other studies by topic, location, or status, go to our Clinical Studies page.

©2021 Primary Aldosteronism Foundation — All Rights Reserved

The Primary Aldosteronism Foundation is a registered 501(c)(3) public charity. Donations are tax deductible in the US.

©2021 Primary Aldosteronism Foundation

The Primary Aldosteronism Foundation is a registered 501(c)(3) public charity. Donations are tax deductible in the US.