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)

There is no doubt that under normal conditions powerful local metabolic regulation adjusts coronary blood flow to myocardial oxygen consumption. However, despite substantial experimental efforts the responsible mediators are still largely unknown. Adenosine, a purported mediator of local metabolic control of coronary blood flow, is probably only involved in transient flow adaptations but not in steady state coronary autoregulation. Even below the autoregulatory range a substantial vasodilator reserve persists, and recruitment of such a vasodilator results in improved regional myocardial blood flow and attenuated regional ischaemic dysfunction. Beta-adrenergic coronary dilation is of minor functional importance. Alpha-adrenergic coronary constriction acts to attenuate increases in coronary blood flow during sympathetic activation under normal conditions, so that myocardial oxygen extraction increases to match the increased oxygen consumption. Alpha-adrenergic coronary constriction remains operative in ischaemic myocardium, thus precipitating or contributing to acute myocardial ischaemia during sympathetic activation and exercise in experimental animals, as well as in patients with stable angina. The vagal transmitter acetylcholine-upon exogenous intracoronary infusion-induces critical constriction of epicardial coronary arteries with endothelial dysfunction and atherosclerosis. However, a vagal initiation of coronary spasm or myocardial ischaemia has not been documented so far. Similarly, peptide hormones/transmitters such as NPY, vasopressin and angiotensin can induce myocardial ischaemia upon exogenous administration. Their pathophysiological role in myocardial ischaemia, however, remains to be established.
 ...
PMID:Control of coronary vasomotor tone in ischaemic myocardium by local metabolism and neurohumoral mechanisms. 166 59

The effects of angiotensin-converting-enzyme (ACE) inhibitors on circulatory regulating mechanisms in congestive heart failure (CHF) were studied by comparison of plasma levels of catecholamines, neuropeptide Y-like immunoreactivity (NPY-LI), substance P (SP-LI), calcitonin gene-related peptide (CGRP-LI), vasopressin (ADH-LI), atrial natriuretic peptide (ANP-LI) and renin activity (PRA) in patients with severe CHF (NYHA III-IV) with (n = 15) or without (n = 17) ACE inhibitors in addition to digoxin and diuretic therapy. Data were also compared with those for healthy subjects (n = 31) and patients with moderate CHF (NYHA I-II). Catecholamines and NPY-LI were increased to the same extent in both groups with severe CHF. CGRP-LI showed no changes relative to controls in any of the patient groups, and was not affected by ACE inhibitors. The SP-LI level was significantly increased in all patient groups. Patients with severe CHF on ACE inhibition had a SP-LI level of 4.05 +/- 0.79 pmol l-1, compared to a concentration of 2.28 +/- 0.30 pmol l-1 (P less than 0.05) in the patient group with a comparable degree of CHF but without ACE inhibition. In the latter group, an inverse relationship appeared between the SP-LI and the serum sodium levels (r = -0.68, P less than 0.05). The patients with severe CHF who received ACE inhibitors had significantly lower ADH-LI levels than the patients with a comparable degree of CHF who were not treated with ACE inhibitors, while the ANP-LI levels was increased to a similar extent in both groups.
 ...
PMID:Increased plasma level of substance P in patients with severe congestive heart failure treated with ACE inhibitors. 171 29

For many years noradrenaline was considered to be the exclusive transmitter released from sympathetic nerves. However, during recent years both ATP and NPY have been suggested to be co-transmitters to noradrenaline in these nerves. The present study aimed to investigate the functional relationship between these suggested transmitters during nerve stimulation with different frequencies and in different extracellular calcium concentrations. Also the importance of the pattern of nerve stimulation and the potentiation of the neurogenic response after a period of high-frequency nerve stimulation were investigated. Contractions caused by nerve stimulation and applied agonists were investigated in segments of small mesenteric arteries from rat. The biophysical, electrophysiological, and pharmacological properties of these vessels are well characterized in previous studies. The rapid contraction caused by a single nerve stimulus, the "single twitch", and the initial, phasic contraction caused by high-frequency nerve stimulation were only slightly affected by alpha-adrenoceptor blockade with prazosin, whereas the tonic response to high-frequency stimulation was markedly reduced. The phasic responses and those to low-frequency nerve stimulation thus appear to be due mainly to a non-adrenergic transmitter. After inhibiting the response to exogenous ATP by alpha beta-methylene ATP, the response to single impulses and to low-frequency nerve stimulation were markedly reduced, while those to high-frequency stimulation were unaffected. This suggests that ATP acts as a true transmitter in sympathetic nerves, being responsible mainly for rapid responses to low-frequency stimulation, and for the initial part of responses to high-frequency stimulation. When alpha beta-methylene ATP and prazosin were given in combination, no contraction was obtained during nerve stimulation at any frequency. However, if in this situation a contraction was induced by e.g. exogenous vasopressin, field stimulation caused a further, slow contraction. This additional response was undoubtedly neurogenic, but required high-frequency nerve stimulation. The response to nerve stimulation was found to be calcium-dependent, the calcium-dependency being more pronounced at low than at high stimulation frequencies. A continuous, high-frequency (8-16 Hz) nerve stimulation could greatly (5-15 fold) enhance the response to subsequent low-frequency nerve stimulation. This potentiation increased with the frequency of the conditioning stimulation and, within limits, with the number of impulses delivered. Also the extracellular calcium concentration during the conditioning stimulation determined the magnitude of the potentiation. This post-tetanic potentiation has many characteristics in common with the post-tetanic potentiation studied in the central and somatomotor nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Neuro-muscular transmission in blood vessels: phasic and tonic components. An in-vitro study of mesenteric arteries of the rat. 197 Feb 12

Adult female rats were i.p. infused (Alzet osmotic minipumps) with neurotensin (NT, 2 micrograms/rat/day for 7 days), arginine-vasopressin (AVP, 2 micrograms/rat/day for 8 days), bombesin (BM, 0.75 microgram/rat/day for 7 days) or injected with neuropeptide Y (NPY, 0.5 microgram/rat twice a day for 4 days). NT infusion increased absolute and relative thyroid gland weight and decreased serum T4 level, while serum TSH and T3 levels remained unchanged. AVP treatment increased thyroid gland weight and serum TSH and T4 levels and a similar effect was induced by prolonged BM infusion. On the other hand, NPY administration had no effect either on thyroid gland weight or on serum TSH, T4 and T3 levels. Results of the present study thus clearly demonstrate a potent stimulatory action of AVP and BM on thyroid gland function and suggest that this effect is mediated by the pituitary gland. On the contrary, prolonged NT infusion decrease serum T4 level while NPY had no effect on thyroid gland function.
 ...
PMID:Effects of prolonged administration of neurotensin, arginine-vasopressin, NPY, and bombesin on blood TSH, T3 and T4 levels in the rat. 210 70

The cytoarchitecture and immunocytochemical distribution of neuropeptides (corticotropin-releasing factor, CRF; neuropeptide Y, NPY; oxytocin, OXY; vasopressin, VP; and vasoactive intestinal polypeptide, VIP) were studied in the hypothalamic suprachiasmatic nuclei (SCN) in male and female ground squirrels of two species (Spermophilus tridecemlineatus and S. richardsonii). Immunoreactive (IR) perikarya were found in sections incubated with VP or VIP antisera. VP-IR cell bodies were seen in the dorsal and medial parts of the nucleus in colchicine-treated animals. IR fibers were distributed throughout the SCN. In the ventral part of the nucleus, VIP-IR cells were seen in untreated animals and were more pronounced in colchicine-treated animals. VIP-IR fibers and terminals form a dense plexus throughout the nucleus. Furthermore, NPY-IR terminals and fibers with multiple varicosities, but no IR perikarya, were present in the suprachiasmatic nuclei. Within the borders of the SCN, no cell bodies or fibers were stained with CRF or OXY antisera in any animal.
 ...
PMID:Immunohistochemical evidence for the presence of neuropeptides in the hypothalamic suprachiasmatic nucleus of ground squirrels. 258 47

a) In the hypothalamus, NPY immunoreactive neurons are non catecholamine containing neurons whereas in the medulla oblongata NPY is present in the majority of the catecholamine neurons. NPY immunoreactive neurons in the MO are critically located at the site of the baroreceptor afferents termination. b) High densities of receptors, as indicated by 125I-pNPY binding studies are present in the various subnuclei of the NTS and area postrema. In slice preparations of this region NPY reduces forskolin and phorbolester-induced cAMP accumulation. c) Antagonistic interactions between NPY-and alpha 2-receptors exist in the NTS. d) Neuropeptide Y and adrenaline both lower the mean arterial blood pressure, heart and respiratory rates after central administration. When given together they antagonize the hypotensive but not the respiratory response of each other. e) Central NPY administration leads to alterations in serum levels of corticosterone, aldosterone, angiotensin II, vasopressin, PRL, LH, GH and TSH which are parallel to changes in discrete hypothalamic catecholamine neuronal systems. f) It is proposed that NPY is a transmitter involved in central cardiovascular and neuroendocrine regulation operating in close association with the CA systems. Before the precise role of NPY can be established, however, specific antagonists have to be developed.
 ...
PMID:Brain neuropeptide Y mechanisms. Basic aspects and involvement in cardiovascular and neuroendocrine regulation. 282 7

Agonist-induced accumulation of [3H]inositol-1-phosphate ([3H]IP1) was studied using human embryonic pituitary tumour cells (Flow 9000). Stimulation of Flow 9000 cells, prelabelled with [3H]inositol, with the nonapeptide bradykinin (BK), or its analogues and fragments produced a differential accumulation of [3H]IP1. BK-related peptides exhibited the following rank order of potency in this assay: BK = [Lys]BK greater than [Met-Lys]Bk much greater than [Des-Arg9]BK much greater than BK(1-6) = BK(2-7) = BK(2-9). BK and [Lys]BK produced half-maximal effects at 2-3 nM. [3H]BK receptor binding studies showed that BK and [Des-Arg9]BK produced a concentration-dependent inhibition of [3H]BK binding with Ki values of 4.8 +/- 1.9 nM (n = 3) and 6.8 +/- 0.7 microM (n = 3) respectively. These studies suggest the presence of B2-bradykinin receptors on the human embryonic pituitary tumour cell-line which appear to be coupled to the phosphatidyl inositol turnover signal transduction mechanism. Cholecystokinin, angiotensin II, vasopressin, thyrotropin-releasing hormone and bombesin also stimulated [3H]IP1 production but were generally much weaker than BK. In contrast, substance P, eledoisin, somatostatin, neurotensin, VIP, NPY, CGRP, U50488, DAGO and DADLE appeared inactive in this system at 10 microM.
 ...
PMID:Bradykinin-induced accumulation of [3H]inositol-1-phosphate in human embryonic pituitary tumour cells by activation of a B2-receptor. 289 11

This paper presents data showing that the sympathetic autonomic areas of the cat thoracolumbar spinal cord contain nerve terminals and fibres with immunoreactivity for at least seven neuropeptides. The distribution in the intermediolateral cell column of the terminals and fibres which contain enkephalin-, neuropeptide Y-, neurotensin-, substance P-, and neurophysin II-like immunoreactivity (ENK, NPY, NT, SP, and NP2, respectively) suggests that these peptides are involved in more generalized functions of the autonomic nervous system. On the other hand, peaks in density of immunoreactivity at certain levels suggest that different levels of influence of sympathetic preganglionic neurons by the various peptides may occur along the length of the thoracolumbar cord. The distribution of terminals and fibres containing somatostatin- and oxytocin-like immunoreactivity (SS and OXY) suggests that these peptides may be part of specific pathways to particular sympathetic preganglionic neurons. The possible sources of the terminals and fibres containing ENK, NPY, NT, SS, and SP include the spinal cord and supraspinal areas, whereas the source of these structures with OXY and NP2 is most likely supraspinal. The data suggest that coexistence of peptides and interactions between structures containing different neuropeptides occur in the spinal autonomic areas. It is speculated that neuropeptides have an important role to play in the regulation of the cardiovascular division of the autonomic nervous system.
 ...
PMID:Peptidergic inputs to sympathetic preganglionic neurons. 331 10

Microelectrode recordings were performed in renin-containing epithelioid (JG) and vascular smooth muscle (VSM) cells of the afferent arteriole in the isolated hydronephrotic mouse kidney. Both cell types had a membrane potential of about -75 mV and exhibited small, spontaneous depolarizing transients, probably resulting from random transmitter release by sympathetic axon terminals. Substances depressing renin secretion, such as angiotensin II, arginine-vasopressin, and alpha 1-adrenergic agents reversibly depolarized both JG and VSM cells. On a molar basis, the action of angiotensin II was strongest. Stimulators of renin release, e.g. isoproterenol, histamine, and prostaglandin E2 did not influence the membrane potential of both cell types. VIP and NPY, possible co-transmitters of norepinephrine, as well as AP II, were also without effect. It is proposed that suppression of renin secretion from JG cells is mediated by depolarization and Ca2+ influx, whereas stimulation is triggered independently from membrane potential changes, e.g. by adenylate cyclase activation.
 ...
PMID:Epithelioid cells: membrane potential changes induced by substances influencing renin secretion. 351 56

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
 ...
PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8


1 2 3 4 Next >>