Disease relevance of

• The possibility has been explored of using a specific angiotensin ii antagonist, saralasin (P-113, 1-sar-8-ala-angiotensin ii) to recognize patients whose hypertension depends upon excessive angiotensin ii activity [1].
• In the conscious two-kidney dog, acute renal artery stenosis increased both arterial pressure and PRA within minutes, and P-113 blocked the rise in pressure associated with the increase in PRA [2].
• In 32 patients P-113 infusion reversibly reduced blood pressure, and almost all of these "P-113 responders" had elevated renal vein and/or peripheral PRA levels, together with evidence of renal ischemia [3].
• These results identify P-113 as a potential antimicrobial agent in the treatment of oral candidiasis [4].
• RESULTS: There was a significant reduction in plaque (p=0.046) and a reduction in gingivitis (p=0.086) for subjects using 0.01% P-113 mouthrinse [5].

High impact information on

• In sodium-restricted dogs (approximately equal to 5 mEq/day), glomerular filtration rate (GFR) also increased with intrarenal P 113 infusion from 57.9 +/- 5.7 to 66.3 +/- 6.6 ml/min (P less than 0.05), and with SQ 20881 infusion from 43.1 +/- 2.1 to 55.7 +/- 4.5 ml/min (P less than 0.01) [6].
• In vitro activity of the histatin derivative P-113 against multidrug-resistant pathogens responsible for pneumonia in immunocompromised patients [7].
• In contrast, P-113D, the mirror-image peptide with the amino acid residues in the D configuration, was stable in sputum, was as active as P-113 against pathogens of CF patients in the absence of sputum and retained significant activity in the presence of sputum from CF patients [8].
• However, P-113 was not active in the presence of purulent sputum from CF patients [8].
• Twenty-five patients in this series had arteriographic renal artery stenosis, of whom 3 had false negative P-113 infusion tests, 9 had negative peripheral renin assays, and 3 had no imaging abnormalities [9].

Biological context of

• C. glabrata was also insensitive to other members of the histatin family; histatin 1, 3 and P-113 (IC50 values in all cases >225 microg/ml) [10].
• The effect of [Sar1, Ala8]angiotensin II (P-113) was compared before and during RAO on blood flow and vascular resistance of the contralateral kidney [11].
• P-113 given intra-arterially to the contralateral kidney consistently increased renal blood flow and decreased RVR during RAO, but did not alter RVR significantly before RAO [11].

Anatomical context of

• Among the 189 "P-113 nonresponders," peripheral PRA was elevated in seven (3.8%), and renal vein PRA ratio was abnormal in two patients, who might represent exceptions to the otherwise successful record of the P-113 response in identifying "angiotensinoginic" hypertensives [3].
• To examine the role of the renin-angiotensin system in aldosterone regulation, P-113 ([Sar1,Ala8]angiotensin II) was infused into the arterial blood supply of the transplanted adrenal gland in conscious sheep [12].

Associations of with other chemical compounds

• 2. In conscious rabbits, infusion of the angiotensin inhibitor, Sar1-Ala8-angiotensin II (P-113), at rates of 0.055, 0.22 or 1.1 nmol min-1 kg-1 into the renal artery, caused dose-related increases in arterial PRA and renal arteriovenous PRA difference [13].
• The screening of renovascular hypertensive patients can be performed on the basis of the blood-pressure response of the patients to saralasin (Sarenin) infusion [14].

Gene context of

• Cleavage was established at Lys5 and His19 of histatin 5, Lys11, Arg12, Phe14, Glu16, Lys17, His18 and Ser20 of dh-5 and Ala4 and Lys11 of P-113 [15].
• For the intent-to-treat population, significantly smaller %BOP changes were noted in subjects treated with 0.0625, 0.125 and 0.375% P-113 gels (17.4, 18.18 and 17.9%, respectively) versus placebo (28.0%) (p < 0.05) at day 29 [16].
• 3. Intravenous infusion of inhibitor P-113, 5.5 nmol min-1 kg-1, into anaesthetized rats produced highly significant increases in PRA and plasma renin concentration without reduction in arterial pressure [13].
• These experiments indicate that during RAO release of renin causes, through formation of angiotensin, an increase in RVR in the contralateral kidney and intra-arterial administration of P-113 restores the vascular resistance to a near-normal level [11].

Analytical, diagnostic and therapeutic context of

• This study indicates that scintigraphy is a useful procedure for the investigation of hypertensive patients when the initial P-113 infusion test is positive, or discordant with other findings [9].
• METHOD: 159 periodontally healthy subjects abstained from oral hygiene procedures and self-administered either 0.005%, 0.01%, 0.05% P-113 or placebo mouthrinse formulations twice daily over a four week treatment period [5].
• 6. An intraventricular perfusion of the angiotensin II receptor-blocking agent P 113 decreases blood pressure in spontaneously hypertensive rats [17].
• Animal studies and human clinical trials showed that P-113 has potential in preventing the development of gingivitis, with no adverse side effects [18].

References