Biomedical subjects

L Share

Publications and source records attributed to L Share.

At least 73 records · Page 4Linked to original sources

PubMed1986

Interrelationship between central bradykinin and vasopressin in conscious rats.

Intracerebroventricular administration of bradykinin (1, 5 and 20 micrograms) into conscious rats resulted in significant dose-dependent increases in the plasma vasopressin concentration, mean arterial blood pressure and heart rate. Peripheral blockade of the pressor action of vasopressin with a vasopressin pressor antagonist (10 micrograms/kg, i.v.) did not cause an attenuation but rather a potentiation and prolongation of the pressor effects of central bradykinin (20 micrograms). Central administration of the vasopressin antagonist (150 ng) caused no peripheral blockade of the pressor effects of exogenous i.v. vasopressin but almost abolished the bradykinin-induced tachycardia, with little effect on the pressor effects of central bradykinin (20 micrograms). The results indicate that centrally administered bradykinin stimulates vasopressin release into the plasma and that central vasopressin may modulate the cardiovascular actions of central bradykinin.

Animals↗

PubMed1986

Osmotic stimulation in DOC-salt hypertension: vasopressin and blood pressure.

To determine whether there is a change in the sensitivity of the osmotic control of vasopressin release in deoxycorticosterone (DOC)-salt hypertension, experiments were performed in unilaterally nephrectomized rats that were either normotensive or were made hypertensive with DOC and given 1% saline to drink. After 3 weeks of treatment, 2.5 mol/l NaCl was infused i.v. into conscious normotensive and hypertensive rats. Increases in both plasma osmolality and plasma vasopressin concentration were similar throughout the course of this infusion in the two groups of rats. Hypertonic saline infusion increased the mean arterial blood pressure in the two groups of rats, but this increase was partially attenuated by the i.v. injection of a vasopressin pressor antagonist. In conclusion, vasopressin release in response to osmotic stimulation was similar in normotensive and hypertensive rats. The pressor response to hypertonic saline in both groups of rats could be partially attributed to the increased plasma vasopressin concentration.

Animals↗

PubMed1986

Central cholinergic control of vasopressin release in conscious rats.

Intracerebroventricular (icv) administration of carbachol into conscious rats evoked a substantial increase in vasopressin secretion and blood pressure in a dose-dependent manner. These effects were blocked by pretreatment with the muscarinic blocker, atropine (10 micrograms icv), but not by the nicotinic blocker, hexamethonium (10 micrograms icv). Hexamethonium did, however, block the increase in blood pressure, the decrease in heart rate, and the very small elevation in the plasma vasopressin concentration induced by nicotine (10 micrograms icv). These results indicate that stimulation of either central nicotinic or muscarinic receptors can affect the cardiovascular system and suggest that the cholinergic stimulation of vasopressin secretion may involve primarily muscarinic receptors in the conscious rat.

Animals↗

PubMed1986

Central adrenergic mechanisms in hemorrhage-induced vasopressin secretion.

The effect of central administration of specific adrenergic agonists and antagonists on hemorrhage-induced vasopressin secretion was studied in conscious rats. The intracerebroventricular (icv) injection of the alpha 2-antagonist yohimbine, the alpha 1-antagonist corynanthine, or the beta-agonist isoproterenol failed to alter the vasopressin or blood pressure responses to two sequential 10% reductions in blood volume. Administration of the beta-antagonist propranolol, however, resulted in a significant attenuation of the vasopressin response to hemorrhage, with little effect on the blood pressure response. The alpha 2-agonist, butylated hydroxytoluene (BHT) 933, caused an enhanced vasopressin response to hemorrhage, with a resulting improved maintenance in blood pressure. The results indicate that both alpha 2- and beta-adrenoreceptors may be involved in the pressure-volume control of vasopressin secretion.

Animals↗

PubMed1986

Methionine-enkephalin and vasopressin in SHR: effects of dehydration.

Enkephalins are found in the posterior pituitary, can alter vasopressin secretion, and have greater pressor effects in spontaneously hypertensive rats (SHR) than in Wistar-Kyoto (WKY) rats. Measurement of the plasma methionine-enkephalin concentration (PMet-Enk) has provided equivocal results in humans and has not been reported in rats. We have developed a highly specific and sensitive Met-Enk radioimmunoassay and determined that Met-Enk circulates in rats but that PMet-Enk is no different between SHR and WKY rats (7.6 +/- 0.8 and 9.2 +/- 0.8 pg/ml, respectively). Water deprivation for 48 h increased the plasma vasopressin concentration (PADH) and 24-h urinary vasopressin excretion (UADHV) in SHR and WKY rats, but PMet-Enk was not altered. There were no differences in PADH and UADHV between SHR and WKY rats in either the euhydrated or dehydrated state. These results suggest that it is unlikely that circulating Met-Enk contributes importantly to the maintenance of hypertension in SHR. There was also no evidence for a greater secretion of vasopressin in SHR than in WKY rats, in contrast to previous reports.

Animals↗

PubMed1986

Central adrenergic control of vasopressin release.

The role of central adrenergic receptors in the control of vasopressin release was studied in the conscious rat. Norepinephrine (10 micrograms) and the alpha-1 agonist, phenylephrine (50 micrograms), administered intracerebroventricularly resulted in significant increases in the plasma vasopressin concentration and blood pressure. The alpha-2 agonist, BHT 933 (50 micrograms) and the beta agonist, isoproterenol (10 micrograms) both caused a significant decrease in the plasma vasopressin concentration with only small changes in blood pressure. The central administration of the alpha-1 antagonist corynanthine (20 micrograms) had no effect on the plasma vasopressin concentration; however, increases in plasma vasopressin levels were observed when either the alpha-2 antagonist yohimbine (20 micrograms) or the beta antagonist propranolol (20 micrograms) were given. It is concluded that central noradrenergic pathways may play an important role in the control of vasopressin release and that this control may involve alpha-1, alpha-2 and beta adrenoreceptors.

Animals↗

PubMed1986

Naloxone does not improve cardiovascular or blunt vasopressin responses in spontaneously hypertensive rats following graded hemorrhage.

The effects of continuous intravenous infusion of naloxone or vehicle on the blood pressure and vasopressin responses to step-wise hemorrhage were examined in conscious, age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). Step-wise hemorrhage progressively lowered blood pressure and increased plasma vasopressin levels in both SHR and WKY. The WKY were relatively resistant to the hypotensive effect of hemorrhage. No significant differences were noted in blood pressure responses between naloxone-treated and vehicle-treated SHR while naloxone treatment attenuated hypotension only slightly in WKY. Plasma vasopressin levels were also elevated by naloxone treatment in SHR following a nonhypotensive hemorrhage equivalent to 0.5% of body weight. However, no differences were observed between plasma vasopressin levels in naloxone-treated and vehicle-treated SHR at greater degrees of hemorrhage. In addition, plasma vasopressin levels were similar at all times in hemorrhaged WKY, regardless of treatment. Plasma vasopressin levels were increased by naloxone in both time-control SHR and WKY. The data demonstrate that naloxone-sensitive systems exert only minimal effects on the immediate cardiovascular responses to hypovolemia in normotensive rats and no measurable effects in SHR. It does appear that naloxone-sensitive mechanisms contribute a small, but significant, tonic inhibitory influence over vasopressin secretion in both normotensive and hypertensive rats under basal conditions and in SHR in response to a small reduction in blood volume.

Animals↗

PubMed1986

Role of brain prostaglandins in the control of vasopressin secretion in the conscious rat.

Administration of 10 micrograms prostaglandin D2 (PGD2), the primary PG identified in the rat brain, into the lateral cerebral ventricle of conscious rats resulted in a significant elevation in the plasma vasopressin (AVP) concentration, without a change in mean arterial blood pressure or heart rate. The central administration of indomethacin (100 micrograms) resulted in a significant attenuation of the AVP response to a peripheral osmotic stimulus (iv 2.5 M NaCl; 100 microliters/kg X min for 30 min), but had little effect on the AVP response to hemorrhage (two successive 10% reductions in the estimated blood volume). Administration of another PG synthetase inhibitor, meclofenamate (100 micrograms, into the lateral cerebral ventricle), resulted in a significant attenuation of the AVP response to both the osmotic stimulus and hemorrhage. It is concluded that brain PGs play a central role in the control of AVP secretion.

Animals↗

PubMed1986

The metabolic clearance rate of and pressor responses to vasopressin in male and female rats.

Recent evidence indicates that the plasma vasopressin concentration is higher in males than in females and that this may be due to sexually dimorphic effects of the gonadal steroids. However, whether this difference in plasma vasopressin levels reflects differences in secretion or metabolism of the hormone could not be determined from the available data. Therefore, we measured the MCR of vasopressin in conscious male and female rats over a broad range of plasma concentrations of the hormone. No differences were observed in MCR either within a sex or between the sexes over the ranges of plasma concentrations of vasopressin tested. This indicates that the differences in basal plasma vasopressin concentration that were previously reported between male and female rats reflect differences in secretion. In addition, the pressor responses to infused vasopressin were 2 to 3 times greater (P less than 0.01) in male than in female rats, even though the plasma vasopressin concentrations achieved in the two groups were identical. Although the basal heart rate was higher (P less than 0.01) in female than in male rats, the decreases in heart rate observed in response to the vasopressin infusions were similar between the sexes. The mechanisms responsible for the differences in basal vasopressin secretion and pressor responsiveness between males and females are uncertain, but could involve actions of the gonadal steroids on the central nervous system and the peripheral vasculature.

Animals↗

PubMed1986

Central atrial natriuretic factor reduces vasopressin secretion in the rat.

Atrial natriuretic factor (ANF, Arg 101-Tyr 126; 0.5 and 2.5 micrograms) administered into the lateral cerebral ventricle of conscious euhydrated and dehydrated rats resulted in a significant reduction in the plasma vasopressin concentration. The effect of ANF on vasopressin secretion was greater in the water-deprived animal. Central ANF was without effect on mean arterial blood pressure in both euhydrated and dehydrated rats. The data suggest that ANF occurring in the central nervous system may be important in the control of vasopressin secretion.

Animals↗

PubMed1986

Vasopressin secretion in normotensive black and white men and women on normal and low sodium diets.

The plasma concentration and the 24-h urinary excretion of vasopressin were studied in normal black and white men and women on a normal sodium (150 mmol/day) diet for 3 days and a low sodium (9 mmol/day; furosemide, 1 mg/kg on first day) diet for 4 days. During the normal sodium diet, the 24-h urinary excretion of vasopressin was significantly (P less than 0.05) higher in men than in women and higher (P less than 0.05) in black than in white subjects. Corresponding differences in plasma vasopressin concentrations (P less than 0.05 to 0.01) were observed, with the exception that the difference between white men and women was not statistically significant. These data suggest that under basal conditions the secretion of vasopressin is higher in men and black subjects than in women and white subjects, although differences in the metabolic clearance of vasopressin cannot be ruled out. Reduction in sodium intake resulted in a significantly (P less than 0.01) decreased excretion of vasopressin in all groups except black women, but had no effect on plasma vasopressin concentrations. Significant (P less than 0.01) differences with respect to sex and race persisted for vasopressin excretion, but not for plasma vasopressin concentrations. Sex- and race-related differences in vasopressin could not be attributed to differences in blood pressure, plasma volume or plasma sodium concentration. The physiological consequences of these differences in vasopressin remain to be determined.

Black People↗

PubMed1985

Platelet and plasma vasopressin in dog during hydration and vasopressin infusion.

Dog platelets contain a substance immunologically similar to arginine vasopressin. In conscious and anesthetized dogs under basal conditions, platelet immunoreactive vasopressin accounts for approximately 40% of the total circulating immunoreactive vasopressin. When the plasma vasopressin concentration in the anesthetized dog was lowered 75% by intravenous infusion of isotonic dextrose solution for 2 h, the platelets failed to discharge a significant quantity of immunoreactive vasopressin. Subsequently, when the plasma vasopressin concentration was elevated to a level 10-fold greater than the initial levels by intravenous infusion of arginine vasopressin, there was no statistically significant increase in the estimated platelet vasopressin content measured 1 and 2 h after the start of the infusion, although there was the suggestion that the platelets had indeed taken up some vasopressin after 2 h of vasopressin infusion. Thus immunoreactive vasopressin in dog platelets does not appear to exchange readily with plasma vasopressin. The physiological role of platelet immunoreactive vasopressin remains to be determined.

Animals↗

PubMed1985

Hemorrhage in DOC-salt hypertensive rats: plasma and platelet vasopressin.

The effect of two consecutive hemorrhages, each 10% of blood volume, on plasma vasopressin concentrations was determined in conscious unilaterally nephrectomized Long-Evans rats made hypertensive by treatment for 3 wk with deoxycorticosterone (DOC) and substitution of 1% saline for drinking water (DOC-salt rats) or DOC alone (DOC rats) and in normotensive unilaterally nephrectomized rats drinking water (H2O rats) or saline (NaCl rats). In response to 20% hemorrhage, blood pressure decreased more (P less than 0.01) and plasma vasopressin increased less (P less than 0.01) in the DOC-salt rats than in the other groups. Under basal conditions, immunoreactive vasopressin was found in the platelets in NaCl, DOC, and DOC-salt rats (P less than 0.01) but not in H2O rats. Platelet vasopressin increased (P less than 0.05-0.01) in response to hemorrhage only in DOC-salt rats. In conclusion, the vasopressin response to hemorrhage in DOC-salt rats is impaired; platelet immunoreactive vasopressin is of little importance in normal rats but is increased by treatment with DOC and/or chronic salt loading; and platelet vasopressin increased in response to hemorrhage only in DOC-salt rats.

Animals↗

PubMed1985

High potassium intake selectively increases urinary PGF2 alpha excretion in the rat.

This study was designed to investigate relationships between dietary potassium and the renal prostaglandin system in rats. The potassium content of the diet was 0.162 mmol/g during the control period and 0.004, 0.162, 1.351, or 2.702 mmol/g during the experimental period. Relative to control data in rats fed a 0.162 mmol/g potassium diet, the urinary excretion of 6-keto-PGF1 alpha was not affected by high potassium intake but increased (P less than 0.05) by 25% in rats fed a low potassium diet for 13 days and was associated with reduction of plasma potassium and with elevation of both plasma renin and net release of 6-keto-PGF1 alpha from renal inner medulla slices incubated in Krebs solution. The excretion of PGF2 alpha was not affected by low potassium intake but increased (P less than 0.05) by about twofold in rats fed a potassium-rich diet (1.351 and 2.702 mmol/g) for 13 days and was associated with elevation of plasma potassium concentration, renal prostaglandin 9-keto-reductase activity, and urinary excretion of kallikrein and vasopressin. The urinary excretion of PGE2 was not altered in rats fed either low or high potassium diets. Altogether, these results indicate selective influence of dietary potassium on the urinary excretion of prostaglandins in the rat.

6-Ketoprostaglandin F1 alpha↗

PubMed1985

Changes in plasma arginine vasopressin during transition from fetus to newborn following minimal trauma delivery of lambs and goats.

Vasopressin in umbilical arterial and venous blood is high at delivery and may be important in the maintenance of arterial pressure and absorption of lung liquid. We used chronically instrumented near-term fetal lambs and goats to investigate the changes in plasma vasopressin that occur during perinatal cardiovascular transition following cesarean section without labor. Plasma arginine vasopressin was more than 5 times greater 15 min following birth than immediately prior to clamping the umbilicus, and it fell progressively over the ensuing 2-5 h to levels not significantly different from before birth. Fifteen min after delivery, neither arterial pressure, blood gases, nor pH appeared to account for the increase.

Animals↗

PubMed1985

Vasopressin release in male and female rats: effects of gonadectomy and treatment with gonadal steroid hormones.

We have found, in normal Wistar rats 10-11 weeks old, that the plasma vasopressin concentration (PADH) and the 24-h urinary excretion of vasopressin (UADHV) were higher in males than in females (P less than 0.01). In rats that were gonadectomized when they were 3 weeks old and studied when they were 10-11 weeks old, PADH and UADHV were reduced in males (P less than 0.01) and increased in females (P less than 0.01 for UADHV; PADH not significant) compared to those in intact males and females, respectively. Treatment of castrated male rats with testosterone tended to increase PADH, but estradiol, progesterone, or a combination of estradiol and progesterone were without effect; UADHV was increased by testosterone (P less than 0.01) and lowered by estradiol plus progesterone (P less than 0.01). In ovariectomized rats, PADH was unaffected by either testosterone or estradiol, but was decreased by progesterone alone (P less than 0.05) or in combination with estradiol (P less than 0.05). In these ovariectomized rats, UADHV was unaffected by testosterone and was decreased by estradiol and progesterone individually or in combination (P less than 0.01). These findings suggest that the gonadal steroid hormones can act either centrally to affect ADH release or peripherally to affect ADH metabolism. Compared to intact male rats, the lower PADH in intact female rats was accompanied by lower urine osmolality and greater urine volume, but further study will be required to appreciate fully the physiological significance of the differing PADH in males and females.

Animals↗

PubMed1985

The presence of methionine-enkephalin in plasma and urine in normal human subjects and various patients.

The present study was performed to investigate whether or not there were enkephalins in plasma and urine in normal subjects and in patients with various diseases. Two kinds of antisera were developed to detect M-enk and L-enk. One has specific affinity with the C-terminus of methionine-enkephalin sulfoxide (M-O-enk), the oxidized form of M-enk, and the other with the N-terminus of L-enk. M-enk-like substance (MELS) was present in blood and urine in normal subjects, but not L-enk-like substance (LELS). Plasma MELS and its urinary output averaged 38 +/- 14 pg/ml (N = 19) and 605 +/- 235 ng/day (N = 15, M. +/- S.D.), respectively. There was a significant increase in plasma MELS and its urinary output in patients with pheochromocytoma. Plasma MELS did not show any significant increase or decrease in Cushing's disease. Addison's disease, panhypopituitarism or chronic glomerulonephritis. The urinary output of MELS was significantly increased in patients with essential hypertension, renovascular hypertension and primary aldosteronism, but was decreased in central diabetes insipidus.

Addison Disease↗

PubMed1985

Increased sensitivity of the osmotic control of vasopressin in sheep with deoxycorticosterone acetate-induced hypertension.

The development of hypertension induced by deoxycorticosterone acetate (DOCA) in sheep was accompanied by increases in both the plasma concentration and the urinary excretion of vasopressin. The vasopressin response to an osmotic stimulus (i.v. infusion of 0.85 mol NaCl/l at 4 ml/min for 75 min) was studied before and after the development of hypertension induced by DOCA in six sheep. Before DOCA implantation, the osmotic stimulus resulted in an increase of plasma osmolality (POSM) from 290 +/- 1 to 303 +/- 1 (S.E.M.) mosmol/kg H2O and in plasma vasopressin concentration (PAVP) from 0.23 +/- 0.04 to 1.07 +/- 0.15 microunits/ml. At least 30 days after DOCA implantation when mean arterial blood pressure had risen from 81 +/- 3 to 117 +/- 5 mmHg, the same osmotic load caused an increase in POSM from 290 +/- 2 to 298 +/- 2 mosmol/kg H2O and PAVP from 0.45 +/- 0.05 to 2.02 +/- 0.27 microunits/ml. POSM and PAVP were significantly correlated in every experiment. However, the slope of the relationship increased significantly (P less than 0.01) after the animals had developed hypertension (0.185 +/- 0.026 vs 0.070 +/- 0.011 (microunits vasopressin/ml)/(mosmol/kg H2O]. The intercepts were similar. After the DOCA implant had been removed osmotic sensitivity returned to normal.

Animals↗