Increase In Vasopressin Concentration Research Articles

Hemodynamic effects in dogs anesthetized with isoflurane and remifentanil-isoflurane

To compare hemodynamic effects in dogs anesthetized with remifentanilisoflurane and with isoflurane alone. 6 adult dogs. Mechanically ventilated, isoflurane-anesthetized dogs received increasing constant rate infusions (CRIs) of remifentanil (0.15, 0.30, 0.60, and 0.90 μg/kg/min) or physiologic saline (0.9% NaCl) solution (control treatment), with a 1-week washout interval between treatments. Each CRI of remifentanil or saline solution was maintained for 60 minutes with equipotent end-tidal isoflurane concentrations that corresponded to 1.3 times the minimum alveolar concentration. Hemodynamic measurements and plasma vasopressin concentrations were determined before and at the end of each CRI and 60 minutes after the end of the infusion regimen. Compared with the control treatment, remifentanil CRIs significantly decreased heart rate (HR) and cardiac index (CI) and significantly increased systemic vascular resistance index (SVRI) and plasma vasopressin concentration. Greatest differences in mean values between treatments were recorded for remifentanil at 0.60 μg/kg/min (HR and Cl were 55% and 47% lower, respectively, and SVRI was 91% higher than for the control treatment). Mean arterial pressure increased significantly during the highest remifentanil CRI (9% higher than for the control treatment). The increase in vascular resistance was positively correlated with increases in vasopressin concentrations (coefficient of determination, 0.65) during anesthesia with remifentanil-isoflurane. Anesthesia maintained with remifentanil-isoflurane may decrease tissue perfusion as a result of a decrease in Cl. However, hypotension may not develop because of systemic vasoconstriction. An increase in plasma vasopressin concentration was associated with the vasoconstriction observed in dogs anesthetized with remifentanil-isoflurane.

Inhibitory effects of different galanin compounds and fragments on osmotically and histamine-induced enhanced vasopressin secretion in rats

The effects of rat, porcine and human galanin, and the human 1–16 and human 16–30 terminal galanin fragments on vasopressin secretion were studied in rat. The plasma vasopressin level was determined by radioimmunoassay (RIA). There were no changes in the basal vasopressin secretion after galanin administration. A significant increase in vasopressin concentration was detected following 2.5% NaCl or histamine administration. I.c.v. injected rat, porcine or human galanin or the 1–16 N-terminal galanin fragment prevented the plasma vasopressin level enhancement. Following the i.v. administration of rat galanin or the i.c.v. injected 16–30 C-terminal galanin fragment, the vasopressin concentration did not return to the normal level. Administration of the galanin antagonist galantid (M15) i.c.v. before the rat galanin i.c.v. injection prevented the inhibitory effect on the increased plasma vasopressin level following 2.5% NaCl solution or histamine administration. The results indicate that there is no significant difference in the inhibitory effect of rat, porcine or human galanin or the 1–16 galanin fragment on the enhanced plasma vasopressin secretion induced by hyperosmosis or histamine administration. Our findings suggest that galanin, as a peptide modulator, is physiologically involved in the regulation of vasopressin release following different forms of stimulation: an osmotic response or histamine administration.

ACE inhibition does not exaggerate the blood pressure decrease in the early phase of spinal anaesthesia

This study investigates whether long-term treatment with an angiotensin converting enzyme inhibitor (ACEI) impairs the hemodynamic regulation during the early phase of spinal anaesthesia. Forty-two patients undergoing minor surgery were studied. Twenty-one patients were long-term treated (ACEI group), while the other patients served as controls (nonACEI group). All patients received a balanced electrolyte solution (6 ml kg(-1)) 20 min before spinal anaesthesia. Mean arterial blood pressure decreased 19% in both groups within 20 min after spinal anaesthesia. Heart rate did not change in either group. Plasma renin concentration increased from 7.3 +/- 2.1 to 12.8 +/- 4 pg ml(-1) during spinal anaesthesia in nonACEI patients (P < 0.05), whereas an elevated plasma renin level remained unchanged in the nonACEI group. The angiotensin II concentration increased in both groups during spinal anaesthesia (P < 0.05). The vasopressin concentration did not change during spinal anaesthesia in the ACEI group, but increased from 1.2 +/- 0.3 to 2.2 +/- 0.5 pg ml(-1) in patients with ACEI treatment (P < 0.05). The norepinephrine concentration increased transiently 5 min after spinal anaesthesia in both groups, and returned to baseline levels within 15 min. Long-term ACEI treatment does not further exaggerate the blood pressure decrease in the early phase of spinal anaesthesia. The increase in vasopressin concentrations in ACEI treated patients seems to be sufficient to compensate for the inhibited renin-angiotensin system. In addition, the transient increase in plasma norepinephrine, which occurs independent of preoperative ACEI treatment, seems to be involved in blood pressure regulation during spinal anaesthesia.

Osmotically‐induced release of vasopressin and oxytocin in non‐pregnant women ‐ influence of estrogen and progesterone

Circulating vasopressin and oxytocin are influenced by ovarian steroid blood levels, but the effect of estrogen and progestogen treatment on induced release of the posterior pituitary hormones is not clear. Eight postmenopausal women who had not been on hormonal replacement therapy for at least two months were included in the study. The women were treated for four weeks with transdermal administration of estradiol-17beta in a daily dose of 100 microg with the addition of 5 mg tablets of medoxyprogesterone twice daily for the last two weeks. A 25 minute intravenous infusion of hypertonic saline (0.06 mg/kg/min) was given before hormonal treatment, and after two and four weeks with serial plasma sampling for assay of vasopressin and oxytocin. The mean basal concentration of vasopressin, which was 0.83+/-0.13 (SE) pmol/L before hormonal treatment, increased to a statistically significant degree after estradiol alone to 1.18+/-0.11 pmol/L and decreased after combined estrogen/progestogen treatment to 0.31+/-0.02 pmol/L. Sodium concentration and osmolality increased in a similar way during all three infusions, but the resultant increase in vasopressin concentration was significantly smaller and slower after treatment with estradiol alone than in the first experiment without pretreatment. The areas under the concentration curve for the second and third infusion were significantly smaller than when no hormone treatment was given. The induced hyperosmolality also caused a rise in oxytocin levels, but no influence of ovarian hormone treatment was observed. Ovarian hormone administration influences vasopressin secretion, affecting both the basal levels in plasma and the responses to an increase in plasma osmolality. The influence of ovarian hormones on oxytocin secretion is minimal.

Analysis of the cardiovascular effects of arginine vasopressin in conscious dogs.

The effects of physiological elevations in arginine vasopressin on the cardiovascular system were studied in a group of nine conscious, chronically instrumented dogs. The animals were studied under normal conditions (plasma vasopressin, 4.1 +/- 0.4 pg/ml), after 24 hours of dehydration (plasma vasopressin, 7.3 +/- 1.5 pg/ml), after a 30-minute vasopressin infusion at 2.6 ng/kg/min (plasma vasopressin, 96.6 +/- 8.1 pg/ml). These increases in vasopressin concentration resulted in no change in arterial pressure and significant changes in the following: a 13 and 29% decrease in resting cardiac output during dehydration and acute infusion, respectively; a 26% reduction in heart rate during acute infusion; a 12 and 54% increase in total peripheral resistance during dehydration and acute infusion; a 16 and 22% reduction in mean circulatory filling pressure during dehydration and chronic vasopressin infusion. In addition, maximum pumping ability of the heart was reduced 16 and 31% during dehydration and acute infusion, respectively. These data suggest that elevations of vasopressin such as those occurring during dehydration or volume depletion potentially may affect cardiovascular performance by three mechanisms: greatly increasing resistance to flow, reducing heart rate, suppressing the pumping ability of the heart.

Excretion of Vasopressin in the Hypoxic Lamb: Comparison between Fetus and Newborn

The factors associated with increased renal excretion of vasopressin (VP) were examined in the hypoxic fetus and newborn. Studies were conducted on six chronically instrumented fetal (117-136 days gestation) and seven newborn lambs (2-6-day-old). Hypoxia was produced by administration of 10% oxygen to the ewe or neonate for 30 min. This procedure caused a 50% reduction in PaO2, no significant change in pHa in either fetus or neonate and a slight fall in PaCO2. Hypoxia caused an increase in VP concentrations in plasma from 1.3 +/- 0.53 to 46.4 +/- 4.71 pg/ml in the fetus and from 5.9 +/- 2.80 to 50.2 +/- 26.68 pg/ml in the neonate. After hypoxia there was a fall in urine output from 0.27 +/- 0.045 to 0.17 +/- 0.046 ml/(min X kg) in the fetus and from 0.15 +/- 0.033 to 0.09 +/- 0.022 ml/(min X kg) in the newborn. The corresponding values for urine osmolality were the following: 168 +/- 30.8 to 325 +/- 30.6 mOsm/kg in the fetus and 388 +/- 65.4 to 523 +/- 51.8 mOsm/kg in the newborn. VP concentration in urine increased from 13 +/- 9.4 to a maximum of 176 +/- 32.4 pg/ml after 30 min of recovery in the fetus and 39 +/- 4.6 to 278 +/- 132.5 pg/ml after 1 h of recovery in the newborn. These levels remained high for at least 1 h after the end of hypoxia. There was a good linear correlation between plasma VP levels and the corresponding urine levels and excretion rates in both the fetus and newborn.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acute vasopressin infusion on blood pressure and plasma angiotensin II in normotensive and DOCA-salt hypertensive rats.

1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min(-1) kg(-1) for 1 hr into normal, sham-operated and DOCA-salt hypertensive rats. Complete vasopressin/blood pressure dose-response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion. 2. DOCA-salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 +/- SD 3.7 fmol/ml) than either the normal (3.9 +/- 2.3, P less than 0.01) or the sham-operated rats (4.5 +/- 2.4, P less than 0.01). 3. The DOCA-salt hypertensive rats did not have my detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups. 4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min(-1) kg(1), when the plasma concentration was between 30 and 40 fmol/ml. 5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22-23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA- salt hypertensive rats (10.5 +/- 2.3, 14.5 +/- 4.5 and 8.0 +/- 1.6 fmol/ml respectively). 6. These findings suggest that the mechanism of vasopressin involvement in DOCA-salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA-salt hypertension may contribute to the suppression of renin and angiotensin II in this state.