Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many patients with high spinal cord injury experience exaggerated blood pressure rises in response to bladder distension. To examine the humoral mechanisms associated with these responses, ECG heart rate, blood pressure and vasoactive hormone levels were measured at baseline and during bladder distension following slow bladder filling in 23 subjects: 9 high spinal lesion patients, 7 low spinal lesion patients and 7 normal control subjects. Systolic blood pressure rose significantly during bladder distension in the high spinal lesion group by an average of 56 mm Hg (48%) and diastolic blood pressure rose by 22 mm Hg (47%), while heart rate fell by a mean of 7.4 beats per minute (15%). By contrast, neither systolic or diastolic blood pressure nor heart rate changed significantly during bladder distension in the low spinal lesion or normal control group. There were no significant changes in plasma levels of noradrenaline, renin, aldosterone, vasopressin, arginine, or atrial natriuretic peptide during bladder distension to account for the blood pressure rise in the high spinal lesion group. These findings suggest that humoral mechanisms are unlikely to play a major role in the mediation of pressor responses to bladder distension in high spinal lesion patients.
 ...
PMID:Cardiovascular and vasoactive hormone responses to bladder distension in spinal and normal man. 159 76

In vitro and in vivo experiments have provided indirect evidence that some of the central actions of angiotensin II (ANG II) involve catecholaminergic pathways in the brain. In this study in conscious rats we investigated the effect of stimulation of periventricular ANG II receptors on blood pressure and on catecholamine release (microdialysis and HPLC) from the paraventricular nucleus (PVN), a hypothalamic area thought to be instrumental in the central pressor responses to ANG II through the release of vasopressin into the blood. Intracerebroventricular (i.c.v.) injections of pressor doses of ANG II (1 ng and 100 ng) led to significant dose-dependent increases of the noradrenaline (NA) release in the PVN (1 ng: 30.95 +/- 6.01 to 47.38 +/- 6.79 pg/sample, P less than or equal to 0.01; 100 ng: 32.93 +/- 5.38 to 73.18 +/- 11.4 pg/sample, P less than or equal to 0.01). These changes coincided in extent and duration with the respective pressor responses. A subpressor dose of ANG II (100 pg) did not release catecholamines from the PVN. Dopamine (DA) and the NA and DA, metabolites 3,4-dihydroxyphenylethylglycol and 3,4-dihydroxyphenylacetic acid, were not influenced by i.c.v. injections of ANG II at any dose. Pretreatment with the novel non-peptide ANG II-AT 1 receptor antagonist DuP 753 (5 micrograms, i.c.v.) abolished the effect of 100 ng ANG II on blood pressure and on NA release. Our results show for the first time in vivo that stimulation of periventricular ANG II-AT 1 receptors induces a selective NA release in the PVN. They further support the hypothesis that ANG II engages a noradrenergic pathway in the PVN to release vasopressin.
 ...
PMID:Angiotensin II evokes noradrenaline release from the paraventricular nucleus in conscious rats. 161 72

The relationship between isometric tension and free cytoplasmic calcium, [Ca2+]i, was investigated in rat isolated resistance arteries using fura-2. Depolarisation with 125 mM K+ induced a tonic contraction, while [Ca2+]i increased transiently but stabilised above resting [Ca2+]i. Furthermore, the tension/[Ca2+]i ratio was lower during activation with 125 mM K+ if the effect of endogenous noradrenaline (NA) was inhibited. Concentration/response curves with NA and K+ indicated that NA increased the sensitivity to [Ca2+]i. Calcium concentration/response curves in the presence of 10 microM NA or 125 mM K+ showed that NA could induce force at or below resting [Ca2+]i, while for any given bath calcium concentration, [Ca2+]i was similar in the presence of NA or K+. Addition of NA or vasopressin (AVP) to vessels depolarised with 125 mM K+ caused force development but no increase in [Ca2+]i, suggesting that agonists increase the efficacy of [Ca2+]i. However, during activation with AVP the efficacy of [Ca2+]i decreased time-dependently. The results suggest that in resistance arteries [Ca2+]i plays a crucial role in excitation-contraction coupling, but the tension/[Ca2+]i relationship can be modified by exogenous and endogenous agonists.
 ...
PMID:Endogenous and exogenous agonist-induced changes in the coupling between [Ca2+]i and force in rat resistance arteries. 161 28

The effect of elevated cerebrospinal fluid Na+ concentration (CSF [Na+]) on the tolerance of blood loss, and concomitant cardiovascular and humoral responses were studied in conscious sheep. A slow (0.7 ml kg-1 min-1) venous haemorrhage was continued until the mean systemic arterial pressure suddenly decreased to less than 50 mmHg, or in the absence of hypotension, until a total blood loss of 25 ml kg-1. Significantly more blood had to be removed to induce hypotension in animals receiving an intracerebroventricular (i.c.v.) infusion (0.02 ml min-1) of 0.5 M NaCl (starting 30 min before haemorrhage and continued throughout the experiment) compared to control haemorrhages without concomitant i.c.v. infusion (22.7 +/- 1.2 ml vs 16.9 +/- 0.9 ml kg-1). In one animal, subjected to 0.5 M NaCl infusion, the blood pressure was still maintained at 25 ml kg-1 of haemorrhage. In spite of a larger blood loss, animals receiving i.c.v. infusion of hypertonic NaCl had an improved recovery of the blood pressure after haemorrhage, due to a better maintained cardiac output rather than to a reinforced increase of the vascular resistance. The improved cardiovascular responses to haemorrhage during elevated CSF [Na+] are not readily explained by the effects on the plasma concentrations of vasopressin, angiotensin II or noradrenaline, although the latter was augmented. The plasma protein concentration decreased already during the 30 min of hypertonic NaCl infusion preceding haemorrhage, and the haemodilution caused by the subsequent blood removal was aggravated, which indicates that this treatment also causes transfer of fluid to the plasma compartment. We conclude that elevated CSF [Na+] increases tolerance to haemorrhage and improves cardiovascular function after blood loss in sheep. Since the haemodynamic responses in many respects were similar to those reported in response to the systemic administration of a small volume of hypertonic NaCl solution in haemorrhagic shock, part of the effect of that treatment may be mediated via cerebral effects of increased Na+ concentration.
 ...
PMID:Increased resistance to haemorrhage induced by intracerebroventricular infusion of hypertonic NaCl in conscious sheep. 163 46

1. During major abdominal surgery there are increases in Factor VIII and plasminogen activator activity, associated with elevated plasma concentrations of vasopressin, of a magnitude shown to affect haemostasis. 2. To investigate the mechanisms involved in the haemostatic response to surgery, 12 patients undergoing fibre-optic colonoscopy were studied, of which six had a complete and six had an incomplete examination. 3. Venous blood samples were taken before, during and after the procedure for assay of plasma vasopressin, adrenaline and noradrenaline concentrations, Factor VIII coagulant activity, von Willebrand factor antigen level, euglobulin clot lysis time, tissue-type plasminogen activator activity and tissue-type plasminogen activator inhibition. 4. In the six patients who underwent a complete procedure the median plasma vasopressin concentration rose from 0.6 pg/ml to 153 pg/ml during colonoscopy. Factor VII coagulant activity rose from 0.9 to 2.4 i.u./ml and von Willebrand factor antigen level rose from 139 to 224%. Plasminogen activator activity increased from 20 to 144 units and tissue-type plasminogen activator activity rose from 107 to 1338 m-i.u./ml, whereas tissue-type plasminogen activator inhibition fell from 4.8 to 1.0 i.u./ml. 5. In the six patients in whom a limited procedure was performed, there were no changes in haemostatic function or in plasma vasopressin concentration. Plasma concentrations of adrenaline and noradrenaline did not change in either group. 6. The results indicate that vasopressin regulates the intrinsic coagulation pathway and fibrinolytic system in the absence of adrenaline release.
 ...
PMID:Haemostatic responses and vasopressin release during colonoscopy in man. 165 70

In endothelial cells of the blood vessels and in other cell types by the cleavage of precursor-molecules 21 amino acids containing peptides--the endothelins--are formed. There exist 3 isoforms. The synthesis of endothelin 1 in the endothelial cells is stimulated by adrenaline, noradrenaline, angiotensin II, arginine-vasopressin, thrombine, interleukin 1 and hypoxia. Receptors for endothelins are distributed in most tissues. A significance of the endothelins apparently exists in the stimulation of the activity of the heart and in the vasoconstriction in the case of a decrease of the blood pressure (when blood is lost) and of hypoxia. Endothelins are also formed in the lungs, the kidneys, the brain and the eye. In experimental animals already a low dose of endothelin has a lethal effect by inducing disturbances in the cardiovascular system. By the snake species Atractaspis engaddensis formed sarafotoxins have a similar structure as the endothelins and are effective by binding to their receptors.
 ...
PMID:[Endothelins--properties, formation, mechanism of action and significance]. 165 17

The periaqueductal gray is a brain region of considerable interest. It is innervated by monoamine-containing neurons as well as by a variety of peptidergic fiber systems, and it participates in the regulation of various functions. Virtually nothing is known about monoamine release in the periaqueductal gray and its receptor-mediated modulation. We therefore studied the release of radioactivity from periaqueductal gray slices preloaded with tritriated monoamines, using an in vitro superfusion method. The release of radioactivity from superfused periaqueductal gray slices after preloading of the tissue with [3H]noradrenaline increased upon electrical stimulation in a frequency-dependent manner. The stimulus-evoked release of radioactivity was Ca(2+)-dependent. Clonidine reduced and yohimbine enhanced the release. The inhibition curve for the effect of clonidine was shifted to the right in the presence of 10(-6) M yohimbine. While phenylephrine, isoprenaline, SK & F 38393, quinpirole, carbachol, [Arg8]vasopressin, alpha-MSH and ACTH-(1-24), at a concentration of 10(-6) M, did not influence the electrically evoked release of radioactivity, [Leu5]enkephalin reduced it. The selective mu-opioid receptor agonists [D-Ala2,NMePhe4,Gly-ol5]enkephalin and [D-Arg2,Lys4]-demorphin-(1----4)-amide reduced the release of radioactivity, whereas the selective delta opioid receptor agonist [D-Pen2,D-Pen5] enkephalin and the selective kappa opioid receptor agonist U-69593 had no effect. In the presence of naloxone, which by itself had no effect on the release of radioactivity, the effect of [D-Arg2,Lys4]dermorphin-(1-4)-amide was abolished. These results show that the release of noradrenaline from periaqueductal gray slices is via a Ca(2+)-dependent exocytotic process, and that it is modulated through alpha 2-adrenoceptors as well as via mu-opioid receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Stimulus-evoked release of tritiated monoamines from rat periaqueductal gray slices in vitro and its receptor-mediated modulation. 165 61

1. Intracellular current and voltage clamp recordings were obtained from rat supraoptic nucleus neurones in superfused hypothalamic explants in order to evaluate their response to dopamine and to D1 and D2 agonists. 2. With one exception, exposure to dopamine (10-200 microM) depolarized supraoptic neurones. When tested for an effect on twenty-one spontaneously active supraoptic neurones, dopamine enhanced the firing of all eleven continuous-firing (possibly oxytocin-secreting) neurones and prolonged the burst in all ten phasic-firing (vasopressin-secreting) neurones. 3. In sixty-seven of sixty-eight neurones where current injection was used to maintain membrane potential below threshold for action potential generation, current clamp data revealed that exposure to dopamine (10-200 microM) was followed in 10-17 s by a gradual 3-7 mV membrane depolarization that lasted for 4-15 min and was accompanied by a 12-23% reduction in input resistance. Exposure to quinpirole, a D2 agonist (10-200 microM), induced a similar response with comparable onset, duration and change in input resistance. In contrast, tests on sixteen cells indicated little or no response to a D1 agonist SKF38393. 4. Under voltage clamp, dopamine was noted to induce an inward current, accompanied by a 7.5-40% increase in membrane conductance over the corresponding time course. 5. Voltage-current plots for dopamine-induced depolarizations were linear in the range -50 to -110 mV. Dopamine and quinpirole depolarizations had extrapolated mean reversal potentials of -25 +/- 10 mV (mean +/- S.D.) and -20 +/- 15 mV respectively. This approximated the mean reversal potential of -20 +/- 8 mV measured from the dopamine-induced inward current using single-electrode voltage clamp. 6. The actions of dopamine were selectively antagonized by two D2 receptor antagonists, sulpiride and spiperone, but neither influenced membrane depolarizations induced by equimolar concentrations of noradrenaline. Dopamine-induced depolarizations also persisted following selective blockade of alpha 1-adrenergic receptors by prazosin; under these conditions, noradrenaline induced membrane hyperpolarization. 7. Following complete substitution of external Na+ with Tris, the reversal potential for the dopamine-induced response was shifted to -70 +/- 9.8 mV. This value was consistently less negative than the estimated potassium equilibrium potential. 8. The depolarization action of dopamine persisted in media containing tetrodotoxin and with an external calcium concentration ([Ca2+]o) of 0 mM-Ca2+ with 6 mM-Mg2+ or Mn2+, but was abolished following intracellular injection of [1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), a Ca2+ chelator.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Dopamine D2 receptor activation depolarizes rat supraoptic neurones in hypothalamic explants. 168 25

A comprehensive study of monoamine transmitter and metabolite concentrations measured by HPLC was undertaken in female (vasopressin-deficient) Brattleboro rats as compared to Long Evans rats. Noradrenaline was significantly increased in 8 out of 13 dissected brain regions, whereas concentrations of the metabolite 3-methoxy-4-hydroxyphenylglycol were not altered. The increases were not restricted to areas which are normally innervated by vasopressin-containing neurons. Serotonin was increased in 6 and dopamine in 4 regions and this was accompanied in some areas by increases in the metabolites 5-hydroxyindolacetic acid and dihydroxyphenylacetic acid. Only in the striatum, cerebellum, and the medulla-pons no changes could be detected in any of the compounds of interest. These results show that the long term absence of vasopressin in Brattleboro rats appears to be associated with increases in monoamine transmitter contents and decreased metabolite/transmitter ratios. The regional distribution of these changes does not bear any relationship to the regional distribution of vasopressin cell bodies or nerve endings.
 ...
PMID:Widespread alterations in central noradrenaline, dopamine, and serotonin systems in the Brattleboro rat not related to the local absence of vasopressin. 169 74

The effects of captopril and of other angiotensin-converting enzyme inhibitors (zofenopril, fosenopril and enalaprilic acid) were tested on the isolated rabbit heart and aorta. Captopril elicited an erratic negative inotropic effect and a reduction in basal coronary perfusion pressure (10(-5)-10(-4) M). The increase of coronary perfusion pressure induced by vasopressin, methoxamine, angiotensin II and Bay K 8644 was partially antagonized by captopril (10(-7)-10(-4) M) in a non-specific manner. These actions were not modified by saralasin or indomethacin and by ex vivo pretreatment with captopril itself. On the aortic strips, the contraction plateau induced by KCl and angiotensin II was partially inhibited (10(-6)-10(-4) M), while no effect was observed on those induced by noradrenaline, serotonin and PGF2 alpha. The Ca2+ concentration-response curve appeared shifted to the right in a non-competitive manner. The other angiotensin-converting enzyme inhibitors showed no effect up to 10(-4) M on isolated heart or aorta. Results obtained with captopril were consistent with vasorelaxant activity independent of the tissue renin-angiotensin system. Modulatory activity on the intracellular calcium movement may be involved.
 ...
PMID:Different effects of captopril and other angiotensin converting enzyme inhibitors on cardiovascular preparations. 174 46


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>