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Environmental management requires new forms of governance, less technical and more deliberative, based on the active involvement of all stakeholders. Geographical dimension can play a central role integrating different scales and themes and supporting collective learning processes. Our scientific community has been studying for several years how to better use physical spatial representations (e.g. maps, pictures, ...) within territorial projects. But understanding actor's cognitive representations of the geographical space of a project is not widely used in an operational way yet. Based on examples derived from three case studies, we present here different survey techniques to study the cognitive spatial representations of individuals. We demonstrate through our examples the diversity of cognitive representations among actors. Biases related to the real space and the languages used to support interactions between the interviewer and the respondent are developed. Beyond the cognitive interest to gather information, we also address the social and relational issues related to this type of survey., La gestion de l'environnement nécessite de nouvelles formes de gouvernance moins technicistes et plus délibératives, basées sur la concertation. La dimension géographique peut jouer un rôle central comme intégrateur entre les échelles et les thématiques et comme support d'apprentissage collectif. Notre communauté travaille depuis plusieurs années sur l'usage raisonné des représentations spatiales dans les projets territoriaux, en particulier les représentations spatiales matérielles (cartes, photos, ...). Par contre, la compréhension des représentations mentales que se font les acteurs de l'espace géographique d'un projet environnemental reste peu exploitée de manière opérationnelle. En nous appuyant sur des exemples tirés de trois études de cas, nous présentons ici les différentes techniques d'enquête pour accéder aux représentations cognitives des acteurs. Nous montrons à travers nos exemples la diversité des représentations qui existent entre les acteurs. Les biais liés à l'espace réel et aux langages utilisés pour supporter l'interaction entre enquêteur et enquêté sont développés. Enfin, au-delà de l'intérêt cognitif de recueil d'information, nous abordons aussi la question des enjeux sociaux et relationnels de ce type d'enquête.

The purpose of these studies was to characterize mechanisms of activation of vascular tissues in order to clarify possible theoretical bases for Ca2+-antagonist (CAt) selectivity. Activation of rabbit aorta, mesenteric artery, and mesenteric resistance vessels by agonists and depolarizing potassium (K+) solution, and inhibition by CAts were studied by measurement of contractions, 45Ca fluxes, and membrane potentials (via intracellular electrodes). We found that the CAts studied (D-600, diltiazem, and nisoldipine) inhibited K+-induced Ca2+ influx and contractions in a closely correlated manner, suggesting inhibition of Ca2+ entry as their primary, if not sole, mechanism of action. Diltiazem and nisoldipine had no effect on intracellular Ca2+ release or on the contractile protein system. The following evidence was obtained to support the tenet that norepinephrine (NE) and 80 mM K+ open two distinct Ca2+ channels, one receptor-operated (ROC) and the other potential-operated (POC): (a) NE activated the rabbit aorta without eliciting a change in membrane potential; (b) NE activation of the rabbit mesenteric resistance vessels was accompanied by membrane depolarization, but this depolarization was blocked by 10(-5) M diltiazem, whereas that induced by 80 mM K+ was not; (c) 45Ca influx stimulated by 80 mM K+ and that stimulated by a maximal [NE] were additive when the two agents were administered together in the aorta and the resistance vessels; (d) the Ca2+-channel agonist Bay K8644 opens the POC but not the ROC in rabbit aorta, as it is capable of stimulating Ca2+ influx in addition to 10(-5) M NE, but not to 80 mM K+; (e) the CAts show selective inhibition of the POC over the ROC in the aorta, whereas diltiazem preferentially inhibits the ROC in the resistance vessels; and (f) alpha adrenoreceptor occupation, phosphodiesterase inhibition, or dibutyryl cyclic AMP selectively inhibits the POC over the ROC in the aorta.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence will be presented in support of the contention that receptor occupation and membrane depolarization open separate Ca2+ channels in rabbit aortic and mesenteric arteriolar smooth muscle. These channels can be differentially activated and inhibited, and the 45Ca influx through these channels is additive. The channels opened by receptor occupation (ROCs) appear to vary markedly among arteries in their sensitivity to organic Ca2+ antagonists, with greatest sensitivity in vessels wherein the release of intracellular Ca2+ by receptor occupation is least. Moreover, within the rabbit aorta, the sensitivity to Ca2+ antagonists is greater at lower rather than at higher concentrations of norepinephrine; this variation in Ca2+ antagonist sensitivity appears also to be inversely related to the degree of release of intracellular Ca2+ by norepinephrine. These observations have led to the hypothesis that the release of intracellular Ca2+ by agonists may decrease the sensitivity of ROCs to Ca2+ antagonists. Direct evidence in support of this hypothesis, however, remains to be obtained.

The dependence of norepinephrine-(NE-) and high potassium (80 mMK) depolarization-induced contractions on extracellular versus intracellular calcium (Ca2+) pools was studied in strips of rabbit superior mesenteric artery and its branches, and in perfused mesenteric resistance vessels. 80 mM K contractions were abolished in the presence of 0 Ca2+ 2 mM EGTA in all arteries studied, whereas 10-5M NE-induced contractions and stimulated 45Ca efflux in 0 Ca2+ 2 mM EGTA decreased in a graded fashion from proximal to distal arteries. These data indicate a decreasing release of intracellular Ca2+ and an increasing dependence on extracellular Ca2+ for NE-induced contractions as one proceeds from proximal to distal arteries. This pattern was paralleled by increasing sensitivity of NE-induced contractions to inhibition by diltiazem (10-9 10-4M) from proximal to distal arteries, while inhibition of 80 mM K contractions was similar in all vessels. 45Ca influx induced by 10-5M NE in the resistance vessels, wherein the NE does not release intracellular Ca2+, is approximately 10,000-fold more sensitive to the action of diltiazem than that in the aorta. However, when the aorta is activated by 10-8 MNE, it becomes more sensitive to inhibition by diltiazem than when it is activated by 10-5 MNE. The former NE concentration does not release intracellular Ca2+ in the aorta, whereas the latter does. Thus, it appears that NE-induced 45Ca influx is most susceptible to inhibition by diltiazem when the NE has not also released intracellular Ca2+. We suggest that the release of intracellular Ca2+ by NE may make its stimulated Ca2+ influx less susceptible to inhibition by diltiazem.

Excitation-contraction coupling in smooth and cardiac muscle can be dis­ rupted by a number of organic compounds known collectively as Ca antago­ nists (CAts). In 1964, Fleckenstein (1) provided the first important clue regarding their possible mechanism of action when he noted that the cardiac effects of two of these agents, verapamil and prenylamine, were similar to those of Ca2+ removal from the extracellular space. A few years later, he proposed that CAts exerted their negative inotropic and coronary vasodila­ tor effects by blocking the entry of Ca2+ into the cells (2, 3). The vasodila­ tor and cardiac effects of CAts are having a great impact on cardiovascular medicine; consequently many reviews and monographs on this subject have appeared in the recent past (4--9). The purpose of this review is to provide an in-depth analysis of the mechanisms of action of CAts, rather than to compile an exhaustive survey of the literature. Only when we know how CAts interact with the processes that regulate Ca availability and sensitivity in smooth muscle can we understand why agents that "antagonize" the action of such a universal intracellular messenger can be effectively de­ ployed as selective therapeutic agents in cardiovascular medicine.

In order to evaluate previously utilized 45Ca influx measurements in Wistar-Kyoto (WKY) rat mesenteric resistance vessels, 45Ca compartments obtained under steady-state conditions have been determined. Curve fitting of 45Ca efflux curves resulting from a 50 min washout of 45Ca from vessels incubated in 45Ca-labeled physiological saline solution (PSS) for 1.5 h yields a biexponential as the best fit. The rapidly exchanging compartment has a t1/2 of 58 +/- 5 s, while the slowly exchanging compartment has a t1/2 of 10.5 +/- 1.5 min. A two-compartment model is proposed, with the rapidly exchanging compartment hypothesized to be extracellularly bound Ca2+, and the more slowly exchanging compartment to be intracellular Ca2+. This model is supported by the observation that high K+ increases the 45Ca content of the slowly exchanging fraction, while decreasing that of the rapidly exchanging fraction. Two components of 45Ca efflux can be further distinguished by washout in ice-cold Ca2+-free PSS containing 2 mM EGTA. Under these conditions, the rapidly lost fraction has a t1/2 of 70 +/- 7 s, while the more slowly lost fraction has a t1/2 of 28.9 +/- 5 min. High K+ also increases the 45Ca content of this fraction. The curve relating the steady-state uptake of 45Ca into this fraction to time can best be fitted to a single exponential, for which the t1/2 and 45Ca content are not different from those determined from steady-state 45Ca efflux data.(ABSTRACT TRUNCATED AT 250 WORDS)