Evaluation of anxiety, salivary cortisol and melatonin secretion following reflexology treatment: a pilot study in healthy individuals.

This pilot study sought to identify an appropriate methodology to investigate the impact of reflexology in healthcare settings. The study involved healthy volunteers to prevent unnecessary intervention to individuals who may already be experiencing health related trauma. Thirty participants underwent either reflexology or no treatment (control), in a cross-over experimental design. Self-reported anxiety (Spielberger STAI), cardiovascular parameters (BP and pulse rate) and salivary cortisol and melatonin concentrations were assessed before and after reflexology. Control data were obtained at the same time points in identical settings. Reflexology had a powerful anxiety-reduction effect ('state'; P<0.001) but no significant effect on underlying anxiety ('trait'). Cardiovascular parameters decreased (P<0.001). Baseline salivary cortisol and melatonin were not significantly correlated with STAI scores and did not change significantly following reflexology. Reflexology reduced 'state' anxiety and cardiovascular activity within healthy individuals, consistent with stress-reduction. Considering the connection between stress/anxiety and well being, the effects of reflexology may have beneficial outcomes for patients. These findings will be transferred to a study involving breast cancer patients where effects may be more pronounced particularly since cancer patients display disregulation of cortisol and melatonin secretion.

Renal response of conscious rats to the simultaneous infusion of glucose and saline.

Conscious male rats received an infusion of glucose in saline (139 mM glucose in 77 mM sodium chloride at 5.2 ml/h) via a tail vein for up to 7 h. A control group of rats received saline alone. Rats of both groups were of similar body weights. Plasma glucose concentration averaged 4.9 +/- 0.4 mmol/l (mean + SEM, n = 5) after 4 h saline infusion and 12.9 +/- 0.2 mmol/l (n = 5; difference, p less than 0.001, paired t-test) after 4 h of combined glucose and saline infusion. Urinary glucose excretion was similar in both groups. Urine flow rate and sodium excretion rate were similar in both groups during the infusions. Calculation of the cumulative changes in sodium balance indicated that both groups of rats returned to sodium balance after about 4 h of infusion and remained so for the subsequent 3 h. Values for plasma protein concentration and plasma osmolality were not significantly different after 4 h of either infusion. Inulin clearance during the 4-6 h period of saline infusion (= 3.40 +/- 0.23 ml/min) was not significantly different to that during the 2-4 h period (= 3.33 +/- 0.20 ml/min). In rats infused with glucose in saline inulin clearance increased significantly during the 4-6 h period compared with that during the 2-4 h period (4.14 +/- 0.32 vs 3.31 +/- 0.32 ml/min, p less than 0.05 paired t-test). Mean arterial blood pressure was similar in the two groups of rats and did not change significantly during the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Dose-response effects of pressor doses of arginine vasopressin on renal haemodynamics in the rat.

1. Dose-response effects of arginine vasopressin on renal haemodynamics were studied in conscious and in pentobarbitone-anaesthetized rats infused with 77 mM-NaCl at 5.2 and 2.6 ml h-1 respectively. 2. Vasopressin at 0.8 pmol h-1 (100 g body weight)-1 did not have a significant effect on arterial blood pressure in conscious or anaesthetized rats. Increasing the dose to 2.5 pmol h-1 (100 g body weight)-1 induced a pressor effect in conscious rats but not in anaesthetized rats. A pressor response was observed in the latter at a dose of 10 pmol h-1 (100 g body weight)-1. 3. Pressor doses of vasopressin of 100 pmol h-1 (100 g body weight)-1 and less did not significantly alter the clearance of p-aminohippurate (PAH) in either conscious or anaesthetized rats. A dose of 1000 pmol h-1 (100 g body weight)-1 significantly decreased PAH clearance in both conscious and anaesthetized animals. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin in both conscious and anaesthetized rats. Moderately pressor doses decreased inulin clearance in conscious animals only. The highest dose administered (1000 pmol h-1 (100 g body weight)-1) decreased inulin clearance in both conscious and anaesthetized rats. 5. Pressor doses of vasopressin had a biphasic effect on the filtration fraction in conscious rats. The filtration fraction decreased with doses of vasopressin at the lower end of the pressor range but increased with the highest dose of 1000 pmol h-1 (100 g body weight)-1. In contrast the filtration fraction did not change significantly with moderate pressor doses in anaesthetized rats but was increased by doses of 100 and 1000 pmol h-1 (100 g body weight)-1. 6. It is concluded that pressor doses of vasopressin lower than 100 pmol h-1 (100 g body weight)-1 do not decrease renal plasma flow rate in conscious or pentobarbitone-anaesthetized rats. The results suggest that the inconsistent effects of vasopressin on renal blood flow reported in the literature are due, at least in part, to the wide range of doses used.

Renal haemodynamic actions of pressor doses of lysine vasopressin in the rat.

1. Dose-response effects of lysine vasopressin on renal haemodynamics were studied in conscious rats infused with 2.5% (w/v) dextrose solution at 5.8 ml/h. 2. Lysine vasopressin was maximally antidiuretic in the absence of a significant pressor effect at a dose of 2.5 pmol h-1 100 g body weight-1. Doses of vasopressin greater than this induced a dose-dependent increase in arterial blood pressure. 3. The clearance of p-aminohippurate (PAH) was not significantly changed by vasopressin, even at pressor doses. Rats pre-treated with indomethacin to inhibit prostaglandin synthesis showed a decrease in PAH clearance during the infusion of vasopressin at a dose of 30 pmol h-1 100 g body weight-1, and this suggests that the renal vasoconstrictor actions of vasopressin are attenuated by dilator prostaglandins. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin but was decreased in a dose-dependent manner by pressor doses. A maximal effect was induced by a dose of 30 pmol h-1 100 g body weight-1 which decreased inulin clearance from 3.23 +/- 0.76 (mean +/- S.E. of mean) to 1.60 +/- 0.37 ml/min (P less than 0.02). A change in inulin clearance (from 3.42 +/- 0.46 to 2.17 +/- 0.33 ml/min, P less than 0.01) was also observed in rats pre-treated with indomethacin and infused with vasopressin at the same dose. The magnitude of the change was not significantly different from that observed in rats which were not treated with indomethacin. 5. Control rats infused with dextrose showed a slight but significant increase in sodium excretion during the course of the experiment. A similar natriuresis was observed in rats infused with non-pressor doses of vasopressin but was considerably enhanced in rats infused with pressor doses of the peptide. The antidiuresis induced by vasopressin remained maximal in rats infused with pressor doses. 6. Potassium and osmolal outputs were unchanged by non-pressor doses of vasopressin but significantly increased during administration of pressor doses. 7. It is concluded that pressor doses of lysine vasopressin do not alter total renal perfusion in conscious rats when the prostaglandin system is intact. Glomerular filtration is, however, decreased in a dose-dependent manner by these amounts but the mechanism is unclear.

Effects of vasopressin-glycine and vasopressin-glycine-lysine-arginine on renal function in the rat.

The peptides vasopressin-Gly and vasopressin-Gly-Lys-Arg occur as part of the sequence of the vasopressin-neurophysin precursor molecule and may be released from the hypothalamus and/or pituitary. [8-Lysine]-vasopressin-Gly (LVP-Gly) and [8-lysine]-vasopressin-Gly-Lys-Arg were administered i.v. to conscious, water-diuretic rats. The renal effects of the peptides were assessed by comparison with the actions of [8-lysine]-vasopressin (LVP) which was administered to separate groups of rats. LVP-Gly and LVP-Gly-Lys-Arg were weakly antidiuretic. LVP-Gly-Lys-Arg was the more potent of the two peptides, but on a molar basis it only had about 10% of the antidiuretic activity of LVP. LVP-Gly and LVP-Gly-Lys-Arg at 10 pmol/h per 100 g body weight (equivalent to the maximal antidiuretic dose of LVP) slightly decreased (P less than 0.001) urine flow without causing significant changes in urine osmolality. LVP (10 pmol/h per 100 g body weight) promoted a marked natriuresis (P less than 0.001) but LVP-Gly and LVP-Gly-Lys-Arg were not natriuretic, even at the dose which was markedly antidiuretic (100 pmol/h per 100 g body weight). Osmolal output decreased at all doses during administration of the extended peptides, but was not significantly changed in the control group or by LVP. Inulin clearance was decreased by about 30% during administration of both LVP and LVP-Gly-Lys-Arg at 100 pmol/h per 100 g body weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Dynamics of glomerular filtration in the river lamprey, Lampetra fluviatilis L.

Hydrostatic pressures decreased in the dorsal aorta (from 21.6 +/- 2.0 to 18.7 +/- 0.2 mmHg), proximal (from 19.5 +/- 1.6 to 16.2 +/- 1.7 mmHg) and distal (from 16.7 +/- 0.7 to 13.2 +/- 0.9 mmHg) renal arteries, and glomerular capillaries (from 16.1 +/- 1.1 to 12.3 +/- 0.6 mmHg) of anesthetized lampreys transferred from freshwater to isosmotic 20-30% seawater. Maximal vascular resistance appeared to be in the efferent arteriole; there was a 67% decrease in pressure between glomerular and peritubular capillaries. Plasma oncotic pressure was unchanged. The calculated afferent effective filtration pressure decreased by 87% after transfer and showed a good correlation with single nephron filtration rate. Effective renal plasma flow was high but variable in freshwater lampreys and decreased by 84% after transfer, but glomerular filtration rate did not decrease proportionately and there was a nonsignificant increase in mean filtration fraction from 0.045 +/- 0.022 to 0.080 +/- 0.021. Calculation of glomerular efferent oncotic pressure indicated that filtration equilibrium did not exist in freshwater lampreys but was attained after transfer. The mean coefficient of filtration of freshwater lampreys was 0.028 +/- 0.002 nl X s-1 X mmHg-1.

Renal extraction and clearance of p-aminohippurate during saline and dextrose infusion in the rat.

The reliability of the use of p-aminohippurate (PAH) as a clearance marker for the determination of renal plasma flow during saline or dextrose infusion was investigated in conscious and anaesthetized rats. In the conscious rat (wt. 350-400 g) infused for 4 h with 0.85% saline followed by 3 h of 2.5% dextrose, PAH clearance averaged 11.50 +/- 1.45 ml/min during saline infusion and 7.83 +/- 0.82 ml/min during dextrose infusion. The difference was significant (P less than 0.02). Inulin clearance, however, was unchanged. With dextrose as the initial infusate, PAH clearance averaged 5.86 +/- 0.65 ml/min and increased (P less than 0.01) to 8.74 +/- 0.71 ml/min following a change of infusate to saline, although inulin clearance was again unchanged. In separate groups of rats anaesthetized with sodium pentobarbitone, a comparison was made between renal blood flow values calculated from PAH clearance and haematocrit, and those determined simultaneously using an electromagnetic flow probe placed on the left renal artery. During 0.85% saline infusion, the calculated value was 88.1 +/- 8.4% of that measured using the flow probe. During 2.5% dextrose infusion the value determined from PAH clearance was only 47.3 +/- 4.2% of that obtained using the flow probe, and this is significantly (P less than 0.01) lower than the ratio found during saline infusion. In another study, renal venous blood samples were obtained from sodium-pentobarbitone-anaesthetized rats during 0.85% saline or 2.5% dextrose infusions, for calculation of the renal PAH extraction ratio. During saline infusion, PAH extraction averaged 68.3 +/- 2.5%, whereas during dextrose infusion PAH extraction was lower (P less than 0.001) and averaged only 48.8 +/- 3.2%. It is concluded that PAH clearance grossly underestimates renal plasma flow during 2.5% dextrose infusion in the rat.

Reduction of urinary excretion of PGE2 and 6 keto PGF1 alpha by tiaprofenic acid.

Tiaprofenic acid (Surgam, Cassenne) was administered intravenously to saline-diuretic conscious rats, at doses of 2, 10 and 25 mg kg-1 body weight. Tiaprofenic acid significantly reduced urinary prostaglandin E2 (PGE2) and 6 keto PGF1 alpha excretion, at all three doses employed. The extent of the reduction was similar for both PGE2 and 6 keto PGF1 alpha output; hence no evidence of 'selectivity' (i.e. sparing of PGI2 synthesis) was observed. Tiaprofenic acid was also administered to rats receiving an infusion of 5% dextrose. The dose employed (0.5 or 1 mg kg-1 body weight) was submaximal and elicited reductions in PGE2 output to values still more than 60% of the control period values. In this group of animals, the percentage change in 6 keto PGF1 alpha excretion was again not significantly different from that of PGE2. The maximal extent of reduction in urinary PGE2 excretion with tiaprofenic acid (25 mg kg-1 body weight) was not significantly different from that elicited by indomethacin (10 mg kg-1 body weight), although the time course of the reduction was different.

Prostaglandin E2 excretion, urine flow and papillary osmolality during saline or dextrose infusion in the conscious rat.

Conscious rats received infusions at 5.8 ml./hr of either 0.9% NaCl or 5% dextrose, via a tail vein, for 6 hr. During this infusion period, urine was collected from the animals, and the urine volume, sodium concentration and immunoreactive PGE2 were determined. Urine flow in both groups was stable during the 2-6 hr period of the infusion and was not significantly different between the two groups. Sodium output was also stable over the 2-6 hr infusion period but obviously the output of the saline-infused group was higher than that of the dextrose-infused group. Urinary PGE2 output was not significantly different between the groups in the 2-4 hr period (79.4 +/- 8.6 p-mole/2 hr in the saline-infused group, 82.1 +/- 5.7 p-mole/2 hr in the dextrose-infused group). In the 4-6 hr period, PGE2 output remained at this level (82.0 +/- 7.8 p-mole/2 hr) in the dextrose-infused group, but fell significantly (to 53.7 +/- 5.0 p-mole/2 hr) in the saline-infused group. In separate groups of animals which received saline or dextrose infusions as above, renal papillary osmolality was determined. The osmolality was significantly (P less than 0.001) higher in the saline-infused group. It is concluded that renal PGE2 synthesis is unlikely to be directly involved in sodium homeostasis and that PGE2 synthesis as measured by urinary PGE2 excretion is not controlled by the papillary osmolality.