Independent action of prostaglandins and kinins on vasopressin-stimulated water flow

Independent action of prostaglandins and kinins on vasopressin-stimulated water flow. The kallikrein-kinin and the prostaglandin systems are both important modifiers of vasopressin action. This study examines whether the systems are dependent on one another for their action. Four groups of toad hemibladders were examined. In groups 1 and 2 animals the endogenous prostaglandin system was inhibited. Inhibition of kallikrein by aprotinin caused vasopressin-stimulated water flow to increase further (24.8 ± 4.9 to 34.5 ± 4.8 µl/min) while potentiation of kinins by captropril caused vasopressin-stimulated water flow to decrease (45 ± 6.3 to 30.5 ± 5.4 µ/min). In groups 3 and 4 endogenous kallikrein was inhibited by aprotinin. The addition of prostaglandin E2 caused vasopressin-stimulated water flow to decrease (17.5 ± 2.7 to 5.71 ± 1.0 µ/min) while the inhibition of endogenous prostaglandins caused vasopressin-stimulated water flow to increase (26.7 ± 3.4 to 39.2 ± 3.5 µ/min). Thus, the inhibitory effects of prostaglandins and kinins on vasopressin-stimulated water flow are independent of one another.Action indépendante des prostaglandines et kinines sur le flux hydrique stimulé par la vasopressine. Les systèmes kallikréine-kinine et prostaglandines sont tous deux d'importants modulateurs de l'action de la vasopressine. Cette étude recherche si ces systèmes sont dépendants entre eux dans leur action. Quatre groupes d'hémi-vessies de crapaud ont été examinés. Chez les animaux des groupes 1 et 2, le système des prostaglandines endogènes a été inhibé. L'inhibition de la kallikréine par l'aprotinine a eu pour effet d'augmenter encore le flux hydrique stimulé par la vasopressine (24,8 ± 4,9 à 34,5 ± 4,8 µ/min), tandis que la potentialisation des kinines par le captopril diminuait le flux hydrique stimulé par la vasopressine (45 ± 6,3 à 30,5 ± 5,4 µ/min). Dans les groupes 3 et 4, la kallikréine endogène était inhibée par l'aprotinine. L'addition de prostaglandine E2 diminuait le flux d'eau stimulé par la vasopressine (17,5 ± 2,7 à 5,71 ± 1,0 µ/min), alors que l'inhibition des prostaglandines endogènes élevait le flux hydrique stimulé par la vasopressine (26,7 ± 3,4 à 39,2 ± 3,5 µl/min). Ainsi, les effets inhibiteurs des prostaglandines et des kinines sur le flux d'eau stimulé par la vasopressine sont indépendants l'un de l'autre

Prevalence of peripheral arterial disease in patients at non-high cardiovascular risk. Rationale and design of the PANDORA study

<p>Abstract</p> <p>Background</p> <p>Lower extremity peripheral arterial disease (PAD) is a marker of widespread atherosclerosis. Individuals with PAD, most of whom do not show typical PAD symptoms ('asymptomatic' patients), are at increased risk of cardiovascular ischaemic events. American College of Cardiology/American Heart Association guidelines recommend that individuals with asymptomatic lower extremity PAD should be identified by measurement of ankle-brachial index (ABI). However, despite its associated risk, PAD remains under-recognised by clinicians and the general population and office-based ABI detection is still poorly-known and under-used in clinical practice. The Prevalence of peripheral Arterial disease in patients with a non-high cardiovascular disease risk, with No overt vascular Diseases nOR diAbetes mellitus (PANDORA) study has a primary aim of assessing the prevalence of lower extremity PAD through ABI measurement, in patients at non-high cardiovascular risk, with no overt cardiovascular diseases (including symptomatic PAD), or diabetes mellitus. Secondary objectives include documenting the prevalence and treatment of cardiovascular risk factors and the characteristics of both patients and physicians as possible determinants for PAD under-diagnosis.</p> <p>Methods/Design</p> <p>PANDORA is a non-interventional, cross-sectional, pan-European study. It includes approximately 1,000 primary care participating sites, across six European countries (Belgium, France, Greece, Italy, The Netherlands, Switzerland). Investigator and patient questionnaires will be used to collect both right and left ABI values at rest, presence of cardiovascular disease risk factors, current pharmacological treatment, and determinants for PAD under-diagnosis.</p> <p>Discussion</p> <p>The PANDORA study will provide important data to estimate the prevalence of asymptomatic PAD in a population otherwise classified at low or intermediate risk on the basis of current risk scores in a primary care setting.</p> <p>Trial registration number</p> <p>Clinical Trials.gov Identifier: NCT00689377.</p

The PANDORA study: peripheral arterial disease in patients with non-high cardiovascular risk.

Few studies are available with sufficient sample size to accurately describe the prevalence of low ankle-brachial index (ABI) in patients at 'non-high' cardiovascular (CV) risk. The aim of this study was to evaluate the prevalence of asymptomatic peripheral arterial disease (PAD), as determined by using ABI, in this patient population. A non-interventional, cross-sectional, pan-European study was conducted in patients with ≥1 CV risk factor in addition to age, evaluating the prevalence of asymptomatic PAD (ABI ≤ 0.90). Secondary objectives included assessing the prevalence and treatment of CV risk factors. Patients were consecutively recruited during scheduled visits to the physician's office, or were randomly selected by the physician from a list of eligible patients. Patients with diabetes were excluded as this condition was deemed to be a secondary prevention risk. 10,287 patients were enrolled (9,816 evaluable: mean age 64.3 years; 53.5% male). Prevalence of asymptomatic PAD was 17.8% (99% CI 16.84-18.83). Factors significantly associated with asymptomatic PAD included hypertension, age, alcohol intake, family history of coronary heart disease, low levels of high-density lipoprotein-cholesterol, and smoking (p < 0.0001). Patients treated with statins were significantly less likely to have asymptomatic PAD than those who were not (odds ratio 0.62; 95% CI 0.50-0.76; p < 0.0001). Asymptomatic PAD was highly prevalent in patients with non-high CV risk, the majority of whom would not typically be candidates for ABI assessment. These patients should be carefully screened, and ABI measured, so that therapeutic interventions known to diminish their increased CV risk may be offered.Journal ArticleResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe