Effect Of SQ Research Articles

Customer Loyalty Islamic Banks in Indonesia: Service Quality Which Mediated by Satisfaction and Customer Trust

Purpose: This study aims to analyze the effect of service quality on loyalty mediated by customer satisfaction and trust. A total of 215 Islamic bank customers in the study area were sampled accidently. Theoretical framework: Theoretically, this study contributes to the gaps in the literature, especially those related to the effect of SQ on Islamic banking loyalty which is mediated by satisfaction and trust simultaneously in one research title. Practically, encouraging Islamic banking management to design SQ programs that integrate the value of satisfaction and trust in the same cultural background to gain customer support and loyalty Design/methodology/approach: There are four latent variables observed; service quality, satisfaction, trust, and loyalty with the number of indicators respectively six, four, three, and four. Data collection was carried out through interviews using a questionnaire. Data were analyzed using Smart-PLS 3.0. The validity test uses factor loading and AVE ( Average Variance Extracted ), the reliability test uses Composite reliability (CR) and Cronbach's Alpha (CA), the direct effect test uses the path analysis matrix, while the indirect effect test uses the specific indirect effects matrix. Findings: The volume of research has been increasing over the past nineteen years, although there are only a few authors, institutions and reference journals contributing to the topic’s consolidation and the countries conducting the most joint research in co- authoring for the largest volume of publications, authors and impact journals. Research, Practical & Social implications: This study concludes that customer loyalty of Islamic banks in Indonesia can be optimized through service quality which is mediated by customer satisfaction and trust. Originality/value: The results of the analysis show that the factor loading value is> 0.6 and the AVE value is> 0.5 which means that the data is valid. CR and CA values > 0.6 which means the data is reliable. The direct effect test shows that service quality, satisfaction and trust have a positive and significant effect (p-value <0.05) on loyalty. Furthermore, service quality has an indirect effect ( specific indirect effects) on customer loyalty through the mediation of satisfaction and trust.

A bovine serum albumin and squaraine dye assembly fluorescent probe for pepsin detection

Gastroesophageal reflux disease (GERD) is a highly prevalent condition. Screening for GERD remains a great challenge due to the non-specific nature of the symptoms. Now, salivary pepsin detection has become an effective tool for diagnosing GERD due to its non-invasive and highly specific advantages. However, the diagnosis of GERD by detecting pepsin in saliva still has factors such as long reaction time, poor selectivity, and low detection sensitivity, which need to be improved. In this work, bovine serum albumin (BSA) and a squaraine dye (SQ) were employed to build a BSA-SQ assembly with a fluorescent “on-off” change for rapid and sensitive detection of pepsin. In a Gly-HCl (pH = 2.6) buffer system, SQ had a significant aggregation caused-quenching (ACQ) effect. As SQ was embedded in the cavity of BSA, this improved its dispersion and inhibited the ACQ effect of SQ, resulting in enhanced fluorescence of the system. At this stage, pepsin catalyzed the hydrolysis of BSA, leading to the aggregation of SQ and the quenching of the fluorescence of BSA-SQ. The high catalytic activity of pepsin makes BSA-SQ suitable for the qualitative and quantitative detection of pepsin, showing a good linear relationship in the range of 0.5–40 μg/mL with a detection limit of 97 ng/mL. Finally, the use of this fluorescent probe method to detect pepsin in human saliva showed results consistent with conventional ELISA methods with relative errors between 0.4 and 5.5 %, confirming the great potential of BSA-SQ for the rapid diagnosis of GERD.

The Role of Customer Trust in Mediating the Effect of SQ and Social Media Marketing on Moderated Converting Intention by Online Customer Referral

The Role of Customer Trust in Mediating the Effect of SQ and Social Media Marketing on Moderated Converting Intention by Online Customer Referral

The Role of Customer Trust in Mediating the Effect of SQ and Social Media Marketing on Moderated Converting Intention by Online Customer Referral

The purpose of this study is to analyze the role of customer trust in mediating the effect of service quality and Social Media Marketing (SMS) on converting intentions moderated by online customer referrals at the state electricity company Meulaboh service unit. The population used in this study were all customers of PLN UP3 Meulaboh, both those who had switched to prepaid and postpaid. The number of samples in this study was 175 people. The sampling technique used is non-probability convenience sampling. Data processing was carried out using SPSS and Amos software using structural equation model (SEM) techniques. The results showed that of the 5 direct influence hypotheses tested, there was one that was not significant, namely the influence of Customer Trust on Converting Intention. The highest coefficient of influence that determines customers switch to prepaid is service quality. This means that customers see the quality of services provided on prepaid both offline and online which is the dominant factor in determining their intention to switch from postpaid to prepaid.

Novel microtubule inhibitor SQ overcomes multidrug resistance in MCF-7/ADR cells by inhibiting BCRP function and mediating apoptosis

The occurrence of multidrug resistance (MDR) is one of the impediments in the clinical treatment of breast cancer, and MDR breast cancer has abnormally high breast cancer resistance protein (BCRP/ABCG2) expression. However, there are currently no clinical drugs that inhibit this target. Our previous study found that 2-Methoxy-5((3,4,5-trimethosyphenyl)seleninyl) phenol (SQ0814061/SQ), a small molecule drug with low toxicity to normal tissues, could target microtubules, inhibit the proliferation of breast cancer, and reduce its migration and invasion abilities. However, the effect and the underlying mechanism of SQ on MDR breast cancers are still unknown. Therefore, in this study, we investigated the effect of SQ on adriamycin-resistant MCF-7 (MCF-7/ADR) cells and explored the underlying mechanism. The MTT assay showed that SQ had potent cytotoxicity to MCF-7/ADR cells. In particular, the results of western blot and flow cytometry proved that SQ could effectively inhibit the expression of BCRP in MCF-7/ADR cells to decrease its drug delivery activity. In addition, SQ could block the cell cycle at G2/M phase in parental and MCF-7/ADR cells, thereby mediating cell apoptosis, which was related with the inhibition of PI3K-Akt-MDM2 pathway. Taken together, our findings indicate that SQ overcomes multidrug resistance in MCF-7/ADR cells by inhibiting BCRP function and mediating apoptosis through PI3K-Akt-MDM2 pathway inhibition.

The Relationship Between Cultural Intelligence (CQ), Spiritual Intelligence (SQ), and Interpersonal Communication Skills: The Case of Cultural Tour Guides

The present study aims to examine the relationship between spiritual intelligence (SQ) and cultural intelligence (CQ) and measure their impacts on interpersonal communication skills on cultural tour guides in a religious complex in Iran via structural equation modeling (SEM). The results of the survey show that there is a positive and significant relationship between SQ and CQ. Also, we found that CQ has a significant effect on interpersonal communication skills. The effect of SQ on communication skills was not supported in this study.

Sanqi Oral Solution Ameliorates Renal Ischemia/Reperfusion Injury via Reducing Apoptosis and Enhancing Autophagy: Involvement of ERK/mTOR Pathways.

Ischemia-reperfusion (I/R) induced acute kidney injury (AKI) is a significant health problem with high morbidity and mortality, yet prophylaxis strategies and effective drugs are limited. Sanqi oral solution (SQ) is a formulated medicine widely used in clinical settings to treat various renal diseases via enriching qi and activating blood circulation while its role on I/R-AKI remains unclear. Herein, by establishing rat I/R-AKI models, we intended to investigate the effect of SQ on the prevention of I/R-AKI and explore its underlying mechanisms. We demonstrated that SQ treatment significantly attenuated renal dysfunction of I/R-AKI, alleviated histological damages, inhibited renal apoptosis, and enhanced autophagy. Further investigation proved that SQ could significantly inhibit the activation of ERK and mTOR signaling pathways. Moreover, its renoprotective effect can be abolished by autophagy inhibitor 3-methyladenine (3-MA). Collectively, our results suggest that SQ exerts renoprotective effects on renal I/R injury via reducing apoptosis and enhancing autophagy, which are associated with regulating ERK/mTOR pathways.

H2S is a key antisecretory molecule against cholera toxin-induced diarrhoea in mice: Evidence for non-involvement of the AC/cAMP/PKA pathway and AMPK

Hydrogen sulphide (H2S) is a gasotransmitter that participates in various physiological and pathophysiological processes within the gastrointestinal tract. We studied the effects and possible mechanism of action of H2S in secretory diarrhoea caused by cholera toxin (CT). The possible mechanisms of action of H2S were investigated using an intestinal fluid secretion model in isolated intestinal loops on anaesthetized mice treated with CT. NaHS and Lawesson's reagent and l-cysteine showed antisecretory activity through reduction of intestinal fluid secretion and loss of Cl− induced by CT. Pretreatment with an inhibitor of cystathionine-γ-lyase (CSE), dl-propargylglycine (PAG), reversed the effect of l-cysteine and caused severe intestinal secretion. Co-treatment with PAG and a submaximal dose of CT increased intestinal fluid secretion, thus supporting the role of H2S in the pathophysiology of cholera. CT increased the expression of CSE and the production of H2S. Pretreatment with PAG did not reverse the effect of SQ 22536 (an AC inhibitor), bupivacaine (inhibitor of cAMP production), KT-5720 (a PKA inhibitor), and AICAR (an AMPK activator). The treatment with Forskolin does not reverse the effects of the H2S donors. Co-treatment with either NaHS or Lawesson's reagent and dorsomorphin (an AMPK inhibitor) did not reverse the effect of the H2S donors. H2S has antisecretory activity and is an essential molecule for protection against the intestinal secretion induced by CT. Thus, H2S donor drugs are promising candidates for cholera therapy. However, more studies are needed to elucidate the possible mechanism of action.

Subcutaneous versus intravenous insulin therapy for glucose control in non-diabetic trauma patients. A randomized controlled trial

Hyperglycaemia in trauma patients admitted to the intensive care unit (ICU) is associated with increased morbidity and mortality. Our pilot study is a prospective randomized controlled trial comparing the impact of two glucose control regimens on outcomes in non-diabetic trauma patients admitted with hyperglycaemia to the ICU. Trauma patients with blood glucose levels (BGLs) ≥7·8 mm within the first 48 h of the hospital admission were randomized to receive intermittent SQ or continuous IV insulin to maintain BGLs between 4·4 and 6·1 mm. We excluded diabetics on the basis of history, or a glycosylated haemoglobin ≥6% on admission. We compared the effect of SQ vs. IV insulin therapy on the ICU length of stay (ILOS). A total of 58 patients were included in the study. The SQ and IV groups were comparable in terms of age, gender, injury severity, revised trauma, Glasgow coma scores and type of trauma (blunt vs. penetrating). There was no significant difference between the two treatment groups in the ILOS (3 vs. 2 days, P = 0·084), hospital length of stay (8 vs. 6, P = 0·09), ventilator support days (6 vs. 3, P = 0·98), requirement for blood transfusion (P = 0·66), rates of infections (P = 0·70), acute kidney injury (P = 0·99) and mortality (P = 0·61). There was no difference between SQ and IV insulin therapy in the ILOS in non-diabetic trauma patients.

RELATIVE CONTRIBUTIONS OF ERα AND ERβ TO REGULATION OF CONSTRICTOR PROSTANOID (CP) FUNCTION IN FEMALE RAT AORTA

Previously, we reported that estrogen enhances CP-potentiated vascular contraction by upregulating expression of COX-2 and thromboxane (TX) synthase. Therefore, the relative roles of estrogen receptor subtypes ERα and ERβ in CP function in female rat aorta were determined. Sprague-Dawley rats were ovariectomized (OvX) or OvX + treated with ER-selective agonists 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN, ERβ) or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl)trisphenol (PPT, ERα), 100 μg/rat/day, 13-16 days). Paired thoracic aortic rings were prepared for isometric tension recording using standard methods, and were pretreated with SQ 29,548 (SQ, 1 μM) or control, and a concentration-response to arginine vasopressin (VP) obtained (10−11−10−6 M). VP-stimulated TX release was measured by RIA of TXB2. Data are means ± S.E. (n = 4 rats/group). Maximal response to VP in OvX (2,485±394 mg/mg ring wt) was unaffected by SQ. PPT enhanced maximal response to VP (4,079±361 mg), which was attenuated by SQ (2,734±429 mg). In contrast, DPN did not alter response to VP (2,187±680) and SQ had no effect. VP-stimulated TX release was similar in PPT (201±23 pg/mg tissue/45 min) and DPN (189±17 pg) but markedly lower in OvX (38±4 pg). In previous studies, 17β-estradiol replacement of OvX rats enhanced aortic response to VP (5,058±193 mg), and restored the attenuating effect of SQ (3,471±206 mg), and increased TX release (91±10 pg). These data suggest that ERα but not ERβ is important in the effect of estrogen to enhance CP-potentiated vascular contraction in female rat aorta. (Supported by TAMU-LSTF).

Pharmacologic profile of the dihydropyrimidine calcium channel blockers SQ 32,547 and SQ 32,926 [correction of SQ 32,946

SQ 32,926 and SQ 32,547, two dihydropyrimidine calcium channel blockers, were characterized as potent inhibitors of depolarization-induced contractions of isolated smooth muscle preparations. In rat aorta, the IC50 values were 5.5 nM for SQ 32,547 and 8.1 nM for SQ 32,926, values which compare favorably with that of 2.9 nM for nifedipine. The dihydropyrimidines were also tested in a model of stable angina: pacing-induced ischemia in dogs. Both SQ 32,547 and SQ 32,926 reduced the ST-segment elevation observed in vehicle-treated animals. No significant changes in hemodynamic status were detected, suggesting that a reduction in cardiac work secondary to afterload reduction was probably not a major contributor to the protective effects. Neither was increased coronary blood flow important for the antiischemic outcome because no significant effects of the dihydropyrimidines were observed on ischemic regional blood flow. SQ 32,547 was also studied in globally ischemic, isolated rat hearts. In this model, SQ 32,547 was protective because it significantly reduced contracture formation and lactate dehydrogenase (LDH) release. Washing out the effect of SQ 32,547 in isolated hearts and smooth muscles was difficult, presumably due to its lipophilicity. In the smooth muscle preparations, the effects of both nifedipine and SQ 32,926 were much more easily washed out. As with other calcium channel blockers, increasing the antiischemic effects of SQ 32,547 was associated with a higher cost in terms of cardiac function. In summary, the two novel dihydropyrimidines, SQ 32,547 and SQ 32,926 showed antiischemic properties in animal models.

Telegammatherapy of advanced malignant neoplasms of the maxillary sinus. A 3-year follow-up of therapeutic results and failures

Early-onset neonatal group B beta-hemolytic streptococcus (GBS) infection exhibits pathophysiologic characteristics of a toxic shock syndrome, in which a cascade of inflammatory mediators are involved. Thromboxane A2 (TXA2) is thought to play an important role as a mediator of the pulmonary response to GBS toxin, because high lung lymph concentrations of a TXA2 metabolite have been observed after GBS toxin injections in sheep. The aim of this study was to evaluate the effects of a selective antagonist of the TXA2-prostaglandin endoperoxide receptor (SQ 29,548). Six unanesthetized young lambs, each serving as its own control, were given SQ 29,548 or vehicle control followed by GBS toxin challenge. Hemodynamic and lung function (lung mechanics, lung volume, ventilation) responses were followed for 5 h. When compared with the control studies, treatment with SQ 29,548 significantly altered the response to GBS toxin. SQ 29,548 reduced the increase in pulmonary and systemic vascular resistance, improved cardiac output and stroke volume, improved dynamic lung compliance but not airway resistance, and improved oxygenation. The attenuating effect of SQ 29,548 was most pronounced during the first phase of toxin response (15-90 min after toxin infusion), but significant treatment effects were also seen during the second phase (120-300 min after toxin infusion). This study demonstrates that TXA2 is an important mediator of the response to GBS toxin and is responsible for hemodynamic and lung function changes. Thromboxane receptor blockade may offer a potential therapeutic approach to infants with severe early-onset GBS sepsis.

Hypotensive effect of a phosphorus-containing novel angiotensin converting enzyme inhibitor, (S)-1-[6-amino-2[[hydroxy(4-phenylbutyl)phosphinyl] oxy]-1-oxohexyl]-L-proline (SQ 29,852) in conscious hypertensive dogs.

The hypotensive efficacy of (S)-1-[6-amino-2[[hydroxy(4-phenylbutyl) phosphinyl]oxy]-1-oxohexyl]-L-proline (SQ 29,852), a phosphorus-containing novel angiotensin converting enzyme inhibitor (ACEI) was examined in conscious two-kidney, one-clip Goldblatt hypertensive dogs. The acute hypotensive effect of SQ 29 852 was compared with that of captopril or enalapril at 3 mg/kg, p.o., for each, and the potencies were ranked as follows, enalapril greater than SQ 29,852 greater than captopril. On the other hand, the hypotension caused by repetitive dosing with SQ 29,852 (3 mg/kg, p.o./d for 7 d followed by another 7-d treatment with 10 mg/kg, p.o./d) was somewhat more marked than that by enalapril at the same dosage. Blood urea nitrogen (BUN) increased in all the animals given enalapril, while that in all of the SQ 29,852-treated animals did not increase. These results indicate that SQ 29,852 is a potent, and long-lasting ACEI with a possible low incidence of side effects.

Anti-Ischemic Activity of the Novel Benzazepine Calcium Antagonist SQ 31,486

We tested the benzazepine, SQ 31,486 for its ability to selectively block the voltage-dependent calcium channel and to protect the ischemic myocardium. SQ 31,486 was found to be a selective calcium antagonist in vascular tissue with an IC50 value of 1.5 microM in KCl-contracted rabbit aorta. SQ 31,486 decreased contractile function and increased coronary flow in nonischemic isolated rat hearts in a concentration-dependent manner. SQ 31,486 also significantly reduced postischemic lactate dehydrogenase (LDH) release and end-diastolic pressure (EDP) compared to vehicle. Reperfusion double product [heart rate (HR) x left ventricular developed pressure (LVDP)] was also significantly improved by SQ 31,486. Diltiazem was a less potent anti-ischemic agent and was significantly more cardiodepressant relative to its anti-ischemic efficacy than was SQ 31,486. Thus, SQ 31,486 should have a larger therapeutic index. In a model of pacing-induced myocardial ischemia in anesthetized, open chest dogs, SQ 31,486 reduced pacing-induced ST-segment elevation approximately 50% at 10, 40, and 70 min after drug administration. This protective effect occurred despite a lack of effect of SQ 31,486 on ischemic regional blood flow and peripheral hemodynamic status.

The Effect of the Thromboxane A2/Prostaglandin Endoperoxide Receptor Antagonist SQ 30,741 on Myocardial Infarct Size and Blood Flow During Myocardial Ischemia and Reperfusion

The effect of the thromboxane A2 (TXA2) receptor antagonist SQ 30,741 on infarct size and myocardial blood flow during coronary occlusion and reperfusion was determined. In anesthetized dogs, the left circumflex coronary artery (LCX) was occluded and after 10 min a continuous infusion of SQ 30,741 (1 mg/kg + 1 mg/kg/h, i.v.) or saline was begun. After 90 min of LCX occlusion, the LCX was reperfused for 5 h and infarct size was then determined. Myocardial blood flows before, during, and after occlusion were determined using radioactive microspheres. SQ 30,741 resulted in a significant decrease in infarct size (34% +/- 6% of left ventricular area at risk) compared to controls (60% +/- 9%). Cardioprotection was also found with SQ 30,741 when infarct size was normalized for both area at risk and predrug collateral flow. The protective effect of SQ 30,741 occurred without an increase in collateral flow. At 1 h postreperfusion, subendocardial flow was significantly higher in SQ 30,741-treated animals (109 +/- 15 ml/min/100 g) compared to controls (71 +/- 16 ml/min/100 g). SQ 30,741, in the dose resulting in infarct size reduction, produced a 95% inhibition of platelet TXA2 receptors throughout the experiment as measured by dose-dependent inhibition of the ex vivo platelet shape change response to U-46,619, a TXA2 mimetic. Thus, a dose of SQ 30,741 that results in TXA2 blockade also results in myocardial salvage without changes in collateral flow.

The role of the renin-angiotensin system in compound 48/80-induced thirst in rats

The role of the renin-angiotensin system in compound 48/80 (3 mg/kg s.c.)-induced thirst in rats was investigated. Bilateral nephrectomy attenuated drinking induced by compound 48/80 but notpolyethylene glycol (PEG) (30%, 5 ml s.c.). Pretreatment with tripelennamine (histamine H1-receptor antagonist, 40 mg/kg i.p.) prior to the administration of compound 48/80 reduced the effect of compound 48/80 on drinking, but pretreatment with cimetidine (histamine H2-receptor antagonist, 40 mg/kg i.p.) or propranolol (β-adrenoceptor antagonist, 10 mg/kg i.p.) had no effect. The effect of SQ 14,225 (angiotensin converting enzyme inhibitor) in various concentrations (0.5–100 mg/kg s.c.) was investigated on the drinking response caused by compound 48/80 (3mg/kg s.c.), PEG (30%, 5 ml s.c.), isoprenaline (0.5 mg/kg s.c.) and hypertonic saline (5.8%, 2 ml s.c.). SQ 14,225 at a dose of 50 mg/kg significantly attenuated the compound 48/80-induced water intake when administered within 30 min prior to the injection of compound 48/80. Pretreatment with a high dose of SQ 14,255 (50 or 100 mg/kg s.c.) 15 min prior to the injection of dipsogens caused inhibition of the drinking response to compound 48/80 or isoprenaline, but not to PEG or hypertonic saline. Pretreatment with lower doses of SQ 14,225 (0.5 or 5 mg/kg, s.c.) had no inhibitory effect on compound 48/80- or isoprenaline-induced water intake. The inhibition of water intake by SQ 14,225 seems to be dependent on the dose and time between administration of SQ 14,225 and compound 48/80 or isoprenaline. Compound 48/80 and hypertonic saline were additively effective in producing the drinking response. The present results suggest that a decrease of plasma volume following plasma extravasation caused by s.c. administration of compound 48/80 may stimulate the juxtaglomerular cells of the kidney to release renin and that the consequent increase of angiotensin in turn stimulates water intake.It is concluded that the renin-angiotensin system makes a contribution to compound 48/80-induced thirst.

Effects of angiotensin-converting enzyme inhibitors on the vascular response to norepinephrine

The effects of three types of angiotensin-converting enzyme inhibitor, SQ 14225 (captopril), SQ 20881 (teprotide) and SA 446 (Santen, Osaka, Japan), on the vascular contraction induced by norepinephrine were studied in the perfused rat mesenteric vascular bed. (1) SQ 14225 attenuated the vascular contraction induced by norepinephrine, but SQ 20881 and SA 446 revealed no effect on vascular reactivity. (2) The effect of SQ 14225 was not altered in the presence of bradykinin or angiotensin II in the perfusate. On the basis of these results, it is suggested that the attenuating effect on the vascular response to norepinephrine may be limited to SQ 14225 and that its effect is not mediated through the renin-angiotensin or kalli-krein-kinin system.

Effect of SQ 14225, an inhibitor of angiotensin I-converting enzyme, on the granulomatous response to Schistosoma mansoni eggs in mice.

Murine schistosomiasis is a granulomatous disease associated with high serum and granuloma angiotensin I-converting enzyme (ACE) activity. SQ 14225, a specific competitive inhibitor of ACE, was administered to normal mice and mice infected with Schistosoma mansoni to determine whether this compound could inhibit granuloma ACE activity and modify the size of the granulomatous response to schistosome eggs. Peroral administration of SQ 14225 for 5 wk to infected mice with peak granulomatous responses decreased ACE activity in isolated liver granulomas. Treated mice demonstrated a decrease in granuloma size in the liver, colon, and ileum, and hydroxyproline concentration of isolated liver granulomas was increased. Mean diameters of synchronous pulmonary granulomas, induced by the pulmonary embolization of schistosome eggs into normal and sensitized mice, were decreased by a similar dose of SQ 14225. Withdrawal of SQ 14225 from unsensitized mice with 2-wk-old synchronous pulmonary granulomas induced an increase in inflammation. Infected, but not normal mice receiving SQ 14225 demonstrated reduced portal pressure, liver weight, and body weight. Both normal and infected mice experienced dipsogenesis, expanded intravascular volume, and increased serum ACE. These observations suggest that SQ 14225 can partially inhibit the granulomatous response to schistosome eggs and the pathological manifestations of schistosomiasis. It is possible that ACE has an inflammatory role in granulomatous inflammation.

Altered blood pressure and renin responses to converting enzyme inhibition after aprotinin-induced kallikrein-kinin-system blockade.

1. The effect of aprotinin-induced blockade of the kallikrein-kinin system on haemodynamic and biochemical responses to converting enzyme inhibition by SQ 14 225 was evaluated in 26 patients with essential hypertension. 2. SQ 14 225 lowered blood pressure in high, normal and low renin hypertension. In low and normal renin patients, but not in high renin patients, the acute blood pressure-lowering effect of SQ 14225 could be overcome by aprotinin. Aprotinin infusion produced small vasopressor effects in all groups of patients. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibitions. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibition. 5. With long-term converting enzyme inhibition kallikrein-kinin system activation seems to play only a minor role. 6. The kallikrein-kinin system may be involved in the regulation of blood pressure. 7. There is no direct evidence of a participation of kallikrein in the activation of prorenin in vivo.

Effects of angiotensin I converting enzyme inhibitor (SQ 14225) on control of aldosterone.

Abstract. To study effects of angiotensin I converting enzyme inhibitor (CEI), SQ 14225, on plasma aldosterone (PA), angiotensin I (AI), angiotensin II (AII), potassium and ACTH were administered with or without the simultaneous injection of SQ 14225 in rabbits. The direct effect of bradykinin on PA was also examined, since it is suspected to augment the action of kinin under the administration of CEI. In rabbits the dose of 1 mg/kg of SQ 14225 by a bolus injection resulted in a marked elevation of plasma renin activity (PRA) and moderate but significant decreases in circulating AII and PA with only a little change of blood pressure. Decrements in circulating AII and those in PA observed after the injection of SQ 14225 were well correlated (r = 0.585, P < 0.05). Stimulatory effects of AII, potassium and ACTH on PA were not affected by SQ 14225, however, those of AI on PA and blood pressure were completely inhibited by pre-treatment of SQ 14225. The infusion of bradykinin showed a remarkable reduction in blood pressure and a small increment in PRA, circulating AII and PA. These results may suggest that the inhibitory effect of acutely administered SQ 14225 on PA is mainly due to the inhibition of conversion from AI to AII, but not direct effects on adrenal glands. Furthermore, it was suggested that the augmented kinin is not related to the inhibitory effect of SQ 14225 on PA. In addition, the administration of SQ 14225 does not change the effects of potassium and ACTH on PA.