Active Citizenship and the Governmentality of Local Lesbian and Gay Politics

This paper explores the relationship between new forums of speakability and continuing unthinkability in the context of British local government lesbian and gay work, particularly post-1997. The paper argues new municipal speech acts ushered in progressive modes of sexual citizenship; at the same time, local government's refusal to think hard, deeply or critically, limited the modes of active citizenship made possible. The paper addresses the easing out of active citizenship through an analysis of local government's self-care and its intensification of firewalls - firewalls which restricted the possibility of certain non-state forces guiding from 'a distance'

Association Between the Natriuretic Action of Angiotensin-(1-7) and Selective Stimulation of Renal Prostaglandin I ₂ Release

Abstract We previously reported that angiotensin-(1-7) [Ang-(1-7)], a heptapeptide derived from the metabolism of either Ang I or Ang II, was biologically active in the rat isolated kidney, producing a marked diuresis and natriuresis that could be dissociated from the modest increase in glomerular filtration rate. The natriuretic response was accompanied by an increase in sodium concentration and concomitant decrease in urinary potassium concentration. Ang-(1-7) has also been shown to stimulate arachidonic acid release from isolated proximal tubules and elicit prostaglandin release from a number of tissues. Therefore, in the present study we tested the hypothesis that prostaglandins participate in the renal actions of Ang-(1-7). Rat isolated kidneys were perfused at 37°C with gassed (95% O 2 /5% CO 2 ) Krebs-Henseleit buffer containing oncotic agents and amino acids for six 10-minute clearance periods at a constant pressure of 90 mm Hg. Ang-(1-7) was infused at a rate that achieved a final concentration of 3 pmol/mL in the presence and absence of 10 μmol/L indomethacin. Prostaglandin E 2 (PGE 2 ) and PGI 2 released into ureteral and venous effluents were measured by enzyme-linked immunoassay. During Ang-(1-7) infusion there was a selective increase in 6-keto-PGF 1α , an index of PGI 2 , appearing in both urine and perfusate; PGE 2 levels were unchanged. Inhibition of stimulated 6-keto-PGF 1α release with indomethacin halved the fourfold increase in urine flow and sevenfold increase in sodium excretion rate without altering the increase in urinary sodium concentration produced by Ang-(1-7). In contrast, the increased potassium excretion rate was unchanged, despite the reduction in urine flow, as indomethacin abolished the fall in urinary potassium concentration caused by Ang-(1-7) infusion alone. Thus, Ang-(1-7) is a specific stimulus for renal PGI 2 versus PGE 2 release. This effect may mediate Ang-(1-7)–induced natriuresis and diuresis and fall in urinary potassium concentration but does not appear to be involved in the doubling of urinary sodium concentration. It is possible that these observations have relevance to the link between prostaglandins and converting enzyme inhibitors in view of earlier reports that these antihypertensive agents substantially increase Ang-(1-7). </jats:p

Role of chloride in the variable response of the kidney to cyclooxygenase inhibition

The role of prostanoids in renal function remains unclear, as inhibitors of cyclooxygenase (COX) have contrasting effects. We postulated that these inconsistencies were related to differential effects of the prevailing chloride concentration on COX-dependent mechanisms. In oncotically perfused rat kidneys, in the presence of either high (117 mM) or low (87 mM) chloride with sodium held constant, low chloride resulted in a higher glomerular filtration rate (GFR) than with high chloride, i.e., 1.2 +/- 0.2 and 0.5 +/- 0.1 ml/min, respectively, for the last clearance period. Water and electrolyte excretion and levels of immunoassayable prostaglandins were higher with low chloride. Indomethacin (10 microM) had opposite effects on renal function depending on the chloride levels, although prostaglandin release was inhibited similarly. For example, indomethacin substantially reduced the elevated urine flow and sodium excretion in the low-chloride group, which, by the last period, were reduced from 111 +/- 32 to 37 +/- 3 microliters/min and 8.3 +/- 2.9 to 3.1 +/- 0.6 mu eq/min, respectively, whereas the lower urine flow and sodium excretion in the high-chloride group increased from 32 +/- 8 to 109 +/- 15 microliters/min and 2.5 +/- 0.8 to 7.1 +/- 1.6 mu eq/min, respectively. In summary, inhibition of COX has differential effects depending on the prevailing chloride concentration, or conversely, high and low chloride have contrasting effects on renal function, which are reversed by COX inhibition. We suggest that prohypertensive and antihypertensive COX-dependent mechanisms are linked to chloride; the latter is an integral component in the development of salt-sensitive hypertension. </jats:p