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 effects of 3 alpha 2-adrenergic receptor agonists on renal function in vasopressin (AVP)-deficient Brattleboro (DI) rats were evaluated. The aim of this study was to determine the relative contribution of central versus peripheral alpha 2-adrenoceptors in mediating diuresis and natriuresis, as well as the role of alpha 2-adrenoceptors in antagonizing the actions of AVP. In addition to the studies of renal function, the effects of AVP deficiency on renal alpha 2-adrenoceptor affinity and number was evalauted along with determination of peripheral catecholamine stores. The centrally acting alpha 2-adrenergic agonists guanabenz and guanfacine significantly increased urine output and sodium excretion in Long-Evans (LE) rats. Guanabenz and guanfacine increased urine output in DI rats but failed to increase sodium excretion. The polar alpha 2-adrenergic agonist, ST-91, increased sodium excretion in both LE and DI rats, however, at a dose of 1.0 mg/kg urine output was significantly decreased in DI rats. The 3 alpha 2-adrenergic agonists increased potassium excretion in LE rats, but at the 1.0-mg/kg dose of guanabenz and ST-91, potassium excretion was significantly inhibited in DI rats. Renal alpha 2-adrenergic receptors and norepinephrine stores were not altered in DI rats. Adrenal NE stores were significantly elevated in DI rats relative to LE rats. The results of this study suggest that in the absence of AVP, centrally acting alpha 2-adrenergic agonists have limited natriuretic action, although peripheral activation of alpha 2-adrenoceptors is sufficient to elicit natriuresis irrespective of the presence of AVP. The chronic deficiency of AVP does not alter renal alpha 2-adrenergic receptor number, but the natriuretic and kaliuretic actions of alpha 2-adrenergic agonists are altered in DI rats.
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PMID:Central and peripheral actions of alpha 2-adrenergic agonists on renal function in Long-Evans and Brattleboro rats. 257 60

The centrally induced effects of angiotensin II and substance P on the cardiovascular system and on neuronal efferent activity of the splanchnic, renal, and adrenal nerves were investigated in chronically instrumented conscious rats. The pressor responses to substance P injected into the lateral brain ventricle were accompanied by marked and short latency increases in heart rate, cardiac output, splanchnic, renal, and adrenal nerve activity, and a rise in plasma noradrenaline and adrenaline. Behaviorally, an arousal-type reaction was observed. In contrast, the pressor responses to intracerebroventricular angiotensin II were associated with initial decreases in heart rate, cardiac output, splanchnic, renal, and adrenal nerve activity, and a fall in plasma noradrenaline at the time of the maximal blood pressure increase. In some but not all animals, a second blood pressure peak associated with increases in heart rate and splanchnic nerve activity was observed after several minutes. Incomplete chronic sinoaortic baroreceptor deafferentiation prevented the angiotensin II-induced fall in heart rate but not the initial fall in splanchnic nerve activity. The decreases in splanchnic nerve activity also occurred in diabetes insipidus rats and persisted in Long Evans rats after vascular vasopressin receptor blockade with d(CH2)5AVP, despite marked reductions of the pressor responses in both groups. Peripheral alpha-adrenoceptor blockade with prazosin or ganglion blockade with hexamethonium inhibited the central angiotensin II pressor responses only in combination with vasopressin receptor blockade. On the other hand, either sympatholytic drug, alone, abolished the pressor responses in the diabetes insipidus rats. This indicates that in intact conscious rats the central pressor effects of angiotensin II are initiated by vasopressin release but become dependent on the sympathetic nervous system when vasopressin is absent or not effective. When rats were allowed to drink in response to angiotensin II, a further sharp rise in blood pressure occurred, together with increases in heart rate and splanchnic nerve activity. The results demonstrate fundamental differences in the mechanisms by which central pressor peptides can influence cardiovascular and autonomic function. It is conceivable that the distinct sympathetic response patterns to central angiotensin II and substance P receptor stimulation form part of a specific cardiovascular adjustment to the individual behavioral reactions, such as drinking, as in the case of angiotensin II, or arousal within the central processing of pain, as in the case of substance P.
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PMID:Differential effects of central angiotensin II and substance P on sympathetic nerve activity in conscious rats. Implications for cardiovascular adaptation to behavioral responses. 257 49

1. This study utilized retrograde anatomical tracer techniques and in vivo extracellular electrophysiological studies to examine caudal ventrolateral and dorsomedial medulla afferents to supraoptic nucleus neurosecretory neurones in male Long-Evans rats. 2. In one series of experiments, pentobarbitone-anaesthetized animals were subjected to ventral exposure of the hypothalamus and rhodamine-tagged latex microspheres (0.05-0.2 microliter) were injected into one supraoptic nucleus. Following perfusion with paraformaldehyde-glutaraldehyde 18-24 h later, cell counts were obtained of rhodamine- and/or catecholamine-labelled neurones in the caudal ventrolateral and dorsomedial medulla both ipsi- and contralateral to the injection site. 3. In the caudal ventrolateral medulla, each injection labelled fewer than 15% of the catecholaminergic neurones; with small injections, most (68-100%) of the rhodamine-labelled neurones also displayed catecholamine histofluorescence. In the caudal nucleus tractus solitarii, one-half to one-third as many rhodamine-labelled cells were observed, but a higher percentage (13-100%) of these were non-catecholaminergic. 4. Extracellular recordings were obtained from antidromically identified supraoptic neurones classified as vasopressin (n = 106) or oxytocin (n = 26) secreting. Single cathodal pulses (0.2 ms duration, 0.02-0.08 mA) applied in the caudal half of the ipsilateral nucleus tractus solitarii evoked a transient (30-50 ms) activation of 63% of both vasopressin- and oxytocin-secreting neurones. Mean latencies (+/- S.E.M.) for vasopressin and oxytocin cells were 49.8 +/- 1.0 and 46.5 +/- 2.4 ms respectively; these were not significantly different. Similar responses were noted to contralateral stimuli applied to four vasopressin and two oxytocin cells. 5. Vasopressin neurones activated by caudal nucleus tractus solitarii stimulation displayed similar patterns of response to stimulation in the caudal ventrolateral medulla. However, latencies from the nucleus solitarius (mean 47.6 +/- 1.4 ms; n = 59) were significantly longer (P less than 0.05) than from the ventrolateral medulla (41.5 +/- 2.0 ms; n = 17). In eight out of eleven vasopressin neurones tested, interruption of synaptic transmission through the ventrolateral medulla reduced or abolished the caudal nucleus tractus solitarii-evoked excitation but had no effect on their response to baroreceptor activation. This manoeuvre affected zero out of five oxytocin cells similarly excited by nucleus solitarius stimulation. 6. These observations indicate that visceral input mediated through the nucleus tractus solitarii is transmitted differentially to supraoptic vasopressin- and oxytocin-secreting neurones.
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PMID:Dorsomedial medulla stimulation activates rat supraoptic oxytocin and vasopressin neurones through different pathways. 262 94

To determine how the vasopressin deficiency in homozygous Brattleboro rats with diabetes insipidus produces increased renin secretion, homozygous and heterozygous Brattleboro rats were infused through subcutaneously implanted Alzet minipumps for 1 wk with a dose of arginine vasopressin that restored plasma vasopressin to normal in the homozygous animals. In the homozygous animals, plasma renin activity (PRA) and the PRA response to immobilization remained elevated compared with Long-Evans controls. Propranolol reduced PRA to normal and markedly reduced the PRA response to immobilization. PRA was normal in heterozygous Brattleboro rats. The data indicate that the increased renin secretion in homozygous rats is a result of increased sympathetic activity, and because circulating vasopressin does not cross the blood-brain barrier, it seems likely that the increased sympathetic activity is central in origin.
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PMID:Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats. 268 67

The incorporation of labeled precursors in phospholipids and glycolipids was studied in discrete brain areas of rats with innate vasopressin deficiency (Brattleboro, DI) and intact Long Evans animals (LE). Tracer incorporation was found to be reduced in septal, hypothalamic and hippocampal phospholipids, but enhanced in the glycolipid fraction isolated from the hypothalamus and hippocampus of Brattleboro rats. The results indicate that inherited vasopressin deficit seems to be associated with altered lipid synthesis in some brain areas of the Brattleboro rat, suggesting a probability for impaired translation of chemical signals.
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PMID:Phospholipid and glycolipid synthesis in brain structures of Brattleboro rats. 269 92

Regional haemodynamic responses to endothelin-1 were assessed in conscious, unrestrained Long Evans rats, chronically instrumented with pulsed Doppler flow probes. Bolus injection of endothelin-1 (0.04 nmol) caused an early transient hypotension and increase in hindquarters vascular conductance. In the presence of NG-monomethyl-L-arginine (L-NMMA), which inhibits endothelial cell nitric oxide production, the hindquarters vasodilator response to endothelin-1 was unchanged and similar to that seen in the presence of vasopressin when the latter was infused to simulate the pressor effects of L-NMMA. These results indicate that the hindquarters vasodilatation in response to endothelin-1 is not dependent upon release of nitric oxide from endothelial cells.
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PMID:NG-monomethyl-L-arginine does not inhibit the hindquarters vasodilator action of endothelin-1 in conscious rats. 269 39

The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.
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PMID:Central oxytocin systems may mediate a cardiovascular response to acute stress in rats. 271 34

The effects of the absence of various hormones (antidiuretic hormone, thyroid hormone, parathyroid hormone, and calcitonin) on proximal and distal structures were studied in diabetes insipidus (DI) Brattleboro rats. The cross-sectional area of the first segment of proximal convoluted tubules (S1) was significantly reduced in thyroparathyroidectomized (TPTX) DI rats compared with Long-Evans rats (the strain of origin of DI rats) and untreated DI rats. Administration of triiodothyronine (T3, 10 micrograms/day for 7 days) to TPTX-DI rats restored the proximal tubule structure. In the distal convoluted tubule (DCT) the cross-sectional area of the epithelium and the number of nuclei per cross-sectional area were significantly greater in untreated ADH-deficient DI rats than in the control Long-Evans rats. Daily administration of 1-desamino-8-D-arginine vasopressin (dDAVP, 500 ng/day for 3 wk) significantly reduced the size and the number of DCT cells in DI rats. Cortical micropuncture data indicated that the Na+ concentration in the fluid delivered to the DCT and the absolute amount of Na+ reabsorbed along the DCT were higher in DI than in dDAVP-treated DI rats. It is concluded that functional changes in the PCT, subsequent to chronic TPTX, are accompanied by marked alteration of the cell anatomy of this nephron segment, and that the processes that modify the Na load delivered to the DCT and the Na transport in the DCT are accompanied by structural modifications of this segment.
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PMID:A structural study of the rat proximal and distal nephron: effect of peptide and thyroid hormones. 271 59

1. Intravenous infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin (DDAVP) were given to conscious, Long Evans rats chronically instrumented with bilateral, common carotid, pulsed Doppler probes and intravascular catheters. 2. During infusion of vasopressin at 0.3 nmol min-1 there was an increase in common carotid vascular resistance with no change in mean blood pressure or heart rate. Following infusion there was a common carotid vasodilatation. 3. During infusion of vasopressin at 3.0 nmol min-1 there were increases in mean arterial blood pressure and in common carotid vascular resistances, accompanied by bilateral reductions in flow and in heart rate. Administration of (+)-(CH2)5Tyr(Et)DAVP (a V1-receptor antagonist), during the continued infusion of vasopressin, reversed the effects of the latter on mean blood pressure and heart rate; under these conditions there were increases in common carotid blood flows above baseline, in company with bilateral vasodilatations. The latter effects persisted after cessation of vasopressin infusion. 4. Infusions of DDAVP were without significant effects on any measured cardiovascular variable. 5. The results do not provide straightforward support for the claim that vasopressin acts to promote cerebral perfusion, at least when V1-receptor effects are unopposed. Furthermore, it seems likely tha the vasodilator influence of vasopressin on the common carotid vascular bed is not due to stimulation of V2-receptors.
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PMID:The effects of infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin on common carotid vascular resistance in conscious, Long Evans rats. 272 Mar 3

Regulation of brain ions and volume in response to 30 min of hypernatremia has been studied in two strains of anesthetized rats, the vasopressin-deficient Brattleboro and its vasopressin-competent parent strain, the Long-Evans. Plasma [Na] was increased by intraperitoneal injection of hyperosmolal NaCl. Brain volume was regulated during hypernatremia associated with tissue uptake of Na and Cl in both strains, but osmotically stimulated uptake of Na was 61% less in the Brattleboro. Blood-to-brain transfer constants for 22Na, measured as a function of plasma osmolality, were similar in the two strains. In contrast, bulk flow of cerebrospinal fluid (CSF) into brain, induced by osmotic dehydration of brain, was 55% less in the Brattleboro. CSF secretion in unstressed animals was also reduced, by 34%, in the Brattleboro compared with the Long-Evans. Reduced Na uptake by the brain of the Brattleboro rat during hypernatremia can be explained on the basis of a three-compartment model of brain volume regulation. Results support a function for vasopressin in brain ion homeostasis.
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PMID:Brain ion and volume regulation during acute hypernatremia in Brattleboro rats. 273 20


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