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

The potential role of adrenaline, both circulating and in the central nervous system, in the maintenance of high blood pressure was examined in stroke-prone spontaneously hypertensive rats (SHRSP). alpha-Monofluoromethyldopa, a long-lasting inhibitor of dopa decarboxylase, was used to induce rapid depletion of central and peripheral catecholamine stores. Subsequent inhibition of phenylethanolamine-N-methyltransferase (PNMT) allowed the gradual restoration of dopamine and noradrenaline but not adrenaline, resulting in a greater relative depletion of adrenaline. Adrenaline was almost totally depleted in the circulation and peripheral tissues. The resting level of blood pressure, however, was unaffected, excepting after administration of a vasopressin (AVP) antagonist. Moreover, there was no reduction in the magnitude of acute pressor responses to electrical stimulation of the rostral ventrolateral medulla oblongata (C1 area), despite extensive loss of adrenaline from the brainstem and spinal cord. The results suggest that adrenaline contributes to the resting level of blood pressure but that its loss can be offset by the pressor activity of AVP. Thus neither central nor peripheral adrenaline stores appear to be essential for the maintenance of hypertension or for centrally-evoked vasoconstriction in adult SHRSP.
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PMID:Effects of depleting central and peripheral adrenaline stores on blood pressure in stroke-prone spontaneously hypertensive rats. 194 21

The effects of various neuroactive substances on the intracellular free Ca2+ concentration ([Ca2+]i) in cultured type-2 astrocytes were examined by fura-2-based microfluorometry. Type-2 astrocytes showed [Ca2+]i elevation in response to all the substances examined, i.e. carbachol (10(-4) M), histamine (10(-4) M), noradrenaline (10(-4) M), serotonin (10(-4) M), substance P (10(-6) M), vasopressin (10(-6) M) and glutamate (10(-4) M). Not all type-2 astrocytes, however, responded to these substances at the concentrations tested, and the percentages of astrocytes showing a Ca2+ response differed depending on the substance. These results indicate that type-2 astrocytes are potential targets for widely diverse neuroactive substances and heterogeneous in response to them.
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PMID:Type-2 astrocytes show intracellular Ca2+ elevation in response to various neuroactive substances. 194 45

Haemodynamic and humoral responses to two subsequent hypotensive haemorrhages, separated by 3 hours and each followed by retransfusion, were studied in unanaesthetized sheep. Haemorrhage was induced by removal of blood from a jugular vein at a rate of 0.7 ml kg-1 min-1 until the mean systemic arterial pressure suddenly decreased by 35 mmHg or more. In addition to the mean systemic arterial pressure, the cardiac output, the mean pulmonary arterial pressure, the central venous pressure and the pulmonary capillary wedge pressure decreased in response to each haemorrhage. The recovery of the systemic and pulmonary arterial pressure was slower and/or less efficient after the second haemorrhage, due to a less pronounced increase of the vascular resistance. Relative bradycardia, in association with the abrupt fall of the mean systemic arterial pressure, was more apparent during the first haemorrhage. The plasma levels of vasopressin, renin activity and angiotensin II were increased by each blood removal, but the vasopressin response to the second haemorrhage was significantly reduced. The plasma noradrenaline concentration was slightly and transiently elevated only in response to the second haemorrhage. The concentration of neuropeptide Y-like immunoreactivity in plasma was unaffected by both haemorrhages. It is suggested that the reduced and delayed increase in the systemic vascular resistance, accompanied by impaired recovery of the arterial pressure, and the relative absence of 'bleeding bradycardia', during the second haemorrhage, were due to the diminished vasopressin response.
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PMID:Haemodynamic and humoral responses to repeated hypotensive haemorrhage in conscious sheep. 195 7

The role of central angiotensin II (AII) in the shaking stress-induced adrenocorticotropic hormone (ACTH), plasma catecholamine secretion and pressor response were investigated using conscious rats. We also studied whether or not vasopressin (VP) is involved in the shaking stress-induced pressor response. The shaking stress caused significant elevations in plasma ACTH, catecholamine, and systolic blood pressure. Intra-third ventricular administration of the AII antagonist, Sar1, Ile8-angiotensin II (saralasin) significantly attenuated pressor response and plasma noradrenaline elevation but not plasma ACTH elevation. Pretreatment with the vascular-type VP receptor (V1) antagonist, d(CH2)5Tyr(Me)AVP, did not attenuate pressor response nor plasma catecholamine elevation. These results indicate that the central angiotensinergic pathway at least partly mediates the shaking stress-induced activation of the sympathetic nervous system without VP involvement, and that central AII does not mediate the ACTH secretion evoked by shaking stress.
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PMID:Role of central angiotensinergic mechanism in shaking stress-induced ACTH and catecholamine secretion. 196 26

Human and pig cystic and pig hepatic arteries were suspended in tissue baths and the effect of alpha-adrenoceptor selective drugs, prostaglandin F2 alpha (PGF2 alpha) and vasopressin were investigated. Prazosin fulfilled the criteria for competitive antagonism in concentrations 10(-9)-10(-7) M. The pA2-values were 9.53 in human cystic, 9.74 in pig cystic, and 9.57 in pig hepatic artery. Rauwolscine had no significant effect in the different arteries. In human cystic artery noradrenaline had significantly (P less than 0.05) higher Emax and pEC50-values (135% of the preceding K(+)-induced contraction and 6.4, respectively) compared with pig cystic (106% and 5.7, respectively) and pig hepatic artery (116% and 5.9, respectively). Vasopressin had no effect in the cystic arteries, whereas it had a high potency (pEC50 was 8.5) but low intrinsic activity (Emax was 14%) in pig hepatic artery. Prostaglandin F2 alpha had a significantly higher Emax in human than in pig arteries. No differences were found in pEC50-values. This study indicates a similarity in pharmacological characteristics of some vasoactive drugs especially between pig cystic and hepatic arteries. If this is also true in man, the easily obtainable cystic artery can be used for screening the effect of drugs on the hepatic artery.
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PMID:Effects of alpha-adrenoceptor active drugs, prostaglandin F2 alpha and vasopressin on cystic and hepatic arteries of pig and man. 196 53

We have studied the neurogenic response of small mesenteric arteries from the rat to evaluate the involvement of possible co-transmitters under various modes of stimulation. Segments of small branches of the mesenteric artery were mounted in a myograph and the intramural nerves were activated with transmural electrical stimulation. A single stimulation of the nerves caused a contraction that was reduced by only 20% in the presence of adrenergic blocking agents (prazosin or phenoxybenzamine), whereas the steady-state response to continuous nerve stimulation of high frequency was reduced by 90-95%. In contrast, all responses to applied noradrenaline in doses up to at least 1 mM were eliminated by phenoxybenzamine treatment. The stable ATP analogue, alpha,beta-methylene ATP, reduced the response to a single nerve stimulation by 70%, but reduced the contraction caused by continuous high-frequency nerve stimulation by only 10%. None of these agents affected the response to applied neuropeptide Y (NPY). The response of relaxed vessels to nerve stimulation was totally blocked by the combination of an adrenoceptor-blocking agent and alpha,beta-methylene ATP, although even in this situation a further neurogenic response could be revealed in vessels precontracted with vasopressin. Responses to either single stimuli or brief burst stimulations were potentiated after high-frequency stimulation. Both the adrenergic and non-adrenergic components were enhanced to roughly the same extent. Also the potentiated response was eliminated by the combined application of prazosin and alpha,beta-methylene ATP. The non-adrenergic transmitter in the sympathetic nerves of small arteries thus appears to be the dominant transmitter during low-frequency nerve stimulation, causing rapid but phasic activation. Noradrenaline is the most important transmitter for higher frequencies, exerting slower but sustained contractions. The post-stimulatory potentiation affects both the adrenergic and the non-adrenergic part of the neurogenic response.
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PMID:Transmitter characteristics of small mesenteric arteries from the rat. 196 20

Haemodynamic and neurohumoral responses to head-up tilt were measured in 28 elderly patients with postural hypotension (EPPH) and 12 healthy elderly subjects (HE). There were no differences in catecholamines between the groups and only noradrenaline increased on tilt (P less than 0.001). Plasma renin activity and aldosterone were similar in HE and EPPH in the supine and tilt positions. In both groups vasopressin increases (P = 0.032), and plasma volume decreases were the same (P = 0.673). Supine EPPH had higher heart rates (P = 0.019) but similar cardiac indices (P = 0.621). Both had similar changes on tilting (P = 0.975 and P = 0.341). Stroke volume decrease was higher in HE (35%) than EPPH (23%; P less than 0.001). HE showed an increase in peripheral resistance on tilting with no change in EPPH (P = 0.005). EPPH had larger coefficients of variation for all variables. The differences in haemodynamic responses and the similarity of neurohumoral responses during tilting suggest end-organ failure in EPPH with individual variations. Postural hypotension in old age is not a single entity.
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PMID:Haemodynamic and neurohumoral responses in elderly patients with postural hypotension. 196 49

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)
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PMID:Neuro-muscular transmission in blood vessels: phasic and tonic components. An in-vitro study of mesenteric arteries of the rat. 197 Feb 12

In individuals above 60 years of age, an age-related decrease in the concentrations of dopamine, noradrenaline, and 5-hydroxytryptamine has been found. This may indicate a neuron loss. As the metabolites are not simultaneously reduced, a compensatory mechanism would seem to exist. In the hypothalamus there are significant positive correlations between the neuropeptides galanin and corticotropin-releasing factor on the one hand, and age over 60 on the other. In brains from patients with dementia of Alzheimer type there are reduced concentrations of cholineacetyl transferase. However, in some brain areas reduced concentrations of 5-hydroxytryptamine, dopamine, and noradrenaline have also been found. The metabolites homovanillic acid and 5-hydroxyindolacetic acid are also reduced. These findings indicate that there is not only a neuron loss in these brains but also a dysfunction of the remaining neurons, reducing the compensatory capacity of the brain. Postmortem investigations of hypothalamus from Alzheimer brains have shown reduced concentrations of 5-hydroxytryptamine. However, the concentrations of galanin, arginin, vasopressin, and somatostatin were significantly increased. The latter may be the result of a disturbed higher control over the hypothalamus. Hypothalamic dysfunction is of interest with regard to the neuroendocrine disturbances seen in Alzheimer-demented patients. Investigations of patients with vascular dementia have suggested the same type of neurotransmitter disturbances as in Alzheimer's disease.
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PMID:Biochemical substrates in normal aging and Alzheimer's disease. 197 Aug 89

We studied whether or not neonatal streptozotocin (STZ) treatment would alter mean arterial pressure (MAP) and blood pressure regulating factors in conscious and unrestrained spontaneously hypertensive rats (SHR). Neonatal STZ administration to SHR resulted in type 2 diabetes mellitus with reduced MAP and heart rate. Plasma glucose was markedly increased in these diabetic animals and was inversely correlated with MAP. In the diabetic SHR, the hypotensive responses to captopril (SQ) or enalapril, administered intravenously, were diminished, regardless of preceding administrations of vasopressin V1-antagonist (AVPA) or hexamethonium (C6), when compared to findings in control rats. In contrast, the C6-induced hypotension was similar in rats with diabetes and control animals. AVPA led to no decrease in MAP in either group. Hypotensive responses to SQ following AVPA and C6 inversely correlated with the plasma levels of glucose in the diabetic group. The combined blockade of the renin-angiotensin system (RAS), sympathetic nervous system and vasoconstrictive action of vasopressin (AVP) abolished the differences in MAP between the groups. Pressor and bradycardic responses to intravenous noradrenaline, angiotensin II and AVP were practically identical in the diabetic and control SHR. Urinary aldosterone excretion rate was not altered by neonatal STZ treatment. In conclusion, a decrease in MAP in SHR with neonatal STZ treatment may be attributed to the suppressed pressor activity of RAS.
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PMID:Suppression of the renin-angiotensin system induced by streptozotocin treatment in neonatal spontaneously hypertensive rats. 197 12


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