No abstract

Intravenous infusion of either epinephrine (5–6 µg/min) or norepinephrine (12–16 µg/min) during maintenance of a constant renal arterial blood pressure by means of suprarenal aortic constriction, or stimulation of the renal nerves produced essentially the same effects on renal function and renal venous plasma renin concentration, the latter being measured indirectly by bioassaying the pressor activity produced by plasma incubation under standardized conditions. Glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion were decreased, and renin concentration was increased. The induction of osmotic diuresis during catecholamine infusion or renal nerve stimulation reversed or prevented the increase in renin secretion but did not alter the changes in GFR or RPF. It is suggested that the increased renin secretion induced by catecholamines and renal nerve stimulation in nondiuretic dogs might be the indirect result of the decrease in filtered sodium produced by these procedures. However, a direct effect of the catecholamines and renal nerves on the renin-secreting cells cannot be ruled out.

The purpose of this study was to determine the effects of a particular psychological stress, exposure to an open-field, on plasma IL-6 activity in rats. Plasma IL-6 activity was 40.6 +/- 7.2 units/ml in control rats, 105 +/- 6.8 units/ml after 30 minutes exposure to an open-field, and 221 +/- 17 units/ml after 60 minutes of exposure (p = 0.0003). There was a positive correlation (r = .71, p = 0.043) between the change in plasma IL-6 activity and body temperature. However, we conclude, based on earlier data relating plasma IL-6 activity to body temperature changes following injection of lipopolysaccharide, that the plasma levels of IL-6 following exposure to an open-field are not high enough to account for the rise in body temperature observed in rats during this stress. In conclusion, these experiments indicate that exposure to psychological stress can elevate the plasma concentration of IL-6, a known mediator of the acute phase response.

Renin concentrations of renal venous plasma were indirectly measured by bio-assaying the pressor activity produced by plasma incubation under standardized conditions. Pressor activity was detectable in 85% of control dogs, was reciprocally related to sodium excretion, but did not correlate with arterial blood pressure. Reduction of mean renal arterial pressure to 90 mm Hg by an aortic clamp decreased sodium excretion and produced sustained increases in renin secretion and arterial blood pressure proximal to the clamp. Release of the aortic clamp resulted in gradual return of these variables toward control values. Induction of diuresis (osmotic diuretics, chlorothiazide, or acetazolamide) prior to aortic clamping minimized or completely prevented the usual clamp-induced rises in renin secretion and proximal blood pressure. Induction of diuresis during aortic clamping returned the elevated renin secretion and proximal blood pressure toward control values. These effects of diuretics could not be explained by changes in renal hemodynamics or plasma composition. Elevation of ureteral pressure in nondiuretic dogs also increased renin secretion and arterial blood pressure. We conclude that renin secretion is not controlled by blood pressure, per se, or intrarenal pressure, but by the flow or composition of intratubular fluid, probably at the level of the macula densa.

The purpose of these studies was to assess whether interleukin 6 (IL-6) is an endogenous pyrogen, responsible for all or part of the fever caused by lipopolysaccharide (LPS) in rats. We have found that the core temperature (as measured by biotelemetry) rose significantly after intracerebroventricular (icv) injection of recombinant human IL-6. The same doses of IL-6, when administered intravenously or intraperitoneally, had no effect on body temperature. The fever caused by icv administration of IL-6 was completely blocked by indomethacin. After injection of fever-inducing doses of LPS, the plasma and cerebrospinal fluid (CSF) IL-6 activities rose, the former much more than the latter. The correlation between fever and plasma IL-6 activity was r = 0.84 (P less than 0.0025); the correlation between fever and CSF IL-6 activity was r = 0.77 (P less than 0.015). The results of this study are consistent with the hypothesis that IL-6 is a mediator of LPS-induced fever in the rat.