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)

In normal persons, a decrease in urine flow following the injection of small amounts of vasopressin was accompanied by a significant decrease in the clearance and excretion of urate. When vasopressin and a small natriuretic dose of mannitol were administered together, urine flow and urate excretion again decreased. The recovery of urine flow to control values was accompanied by a similar recovery of urate excretion. Because a natriuretic dose of mannitol did not reverse the antiuricosuric effect of the flow decline, it is postulated that the flow effect probably reflects changes in a component of urate efflux distal to the loop of Henle.
Nephron 1976
PMID:Variation of urate excretion with urine flow in normal man. 124 65

Retinal capillary pericytes are believed to have a contractile function and to regulate retinal blood flow at the microvascular level. Membrane potential is an important control element for contractility in smooth muscle cells. In the present study, bovine retinal capillary pericytes have been grown in tissue culture and membrane potentials have been measured using glass microelectrodes. Resting potentials averaged -31 +/- 7 mV (n = 203). Relative K+ conductance was low, with a transference number for K+ of 0.16. Readdition of K+ to K(+)-depleted cells transiently hyperpolarized the membrane potential, probably by stimulating the electrogenic Na+/K+ transport. Repetitive spike-like depolarizations (action potentials) were induced by stimulating the Na+/K(+)-ATPase, by applying norepinephrine (10(-5) mol/l), and by adding 10 mmol/l Ba2+. These action potentials depended on the presence of extracellular Ca2+ and were inhibited by the Ca2+ antagonist nifedipine (10(-6) mol/l). Norepinephrine (10(-5) mol/l) depolarized the membrane by 7.4 +/- 3.5 mV (mean +/- SD, n = 49). This response was blocked by the alpha 1-antagonist prazosin (10(-5) mol/l). Histamine also led to a membrane depolarization of 8.6 +/- 2.8 mV (n = 49), which could be inhibited by the H1-antagonist diphenhydramine. Endothelin (10(-7) mol/l), vasopressin (10(-6) mol/l), and acetylcholine (10(-4) mol/l) had no major effects on membrane potential. The conclusion is that retinal capillary pericytes are excitable cells and react to several vasoactive substances.
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PMID:Membrane potentials in retinal capillary pericytes: excitability and effect of vasoactive substances. 131 66

The renal effects of acyclovir (100 mg/kg body weight i.p. for 7 days) were studied in rats. All animals became polyuric and presented an increase in blood urea nitrogen and fractional excretion of sodium and potassium. During hypotonic saline infusion, the acyclovir-treated rats showed higher distal fractional delivery compared to normal rats (27.8 +/- 4.7 vs. 11.3 +/- 0.9%, p less than 0.01) and a lower ratio of free-water clearance to distal sodium delivery (33.5 +/- 7.8 vs. 57.2 +/- 3.9%, p less than 0.02). Following hypertonic saline infusion, the ratio of osmolar to inulin clearance was higher in acyclovir rats (47.8 +/- 7.4%) than in normal rats (27.0 +/- 4.8%), whereas the ratio of free-water reabsorption to osmolar clearance was lower in the acyclovir rats (13.6 +/- 4.6 vs. 38.2 +/- 3.2%, p less than 0.01). These findings suggest an effect of acyclovir on the proximal tubule, thick ascending limb and/or inner medullary collecting duct (IMCD). In vitro measurements of 3H2O permeability of perfused IMCD of normal rats showed that vasopressin (50 microU/ml) added to the bath increased the diffusional water permeability (43.4 +/- 4.8 vs. 105.6 +/- 9.1 x 10(-5) cm/s), while in acyclovir rats, the control value (58.8 +/- 9.1 x 10(-5) cm/s) did not increase significantly in the presence of vasopressin (71.3 +/- 13.6 x 10(-5) cm/s). These results suggest that high doses of acyclovir produce azotemia and an abnormal function of the proximal tubule and thick ascending limb associated with resistance to vasopressin of the IMCD.
Nephron 1992
PMID:Effects of acyclovir on renal function. 143 96

The kidney involvement in leptospirosis appears to be a special form of acute renal failure due to a higher frequency of polyuric forms and the presence of hypokalemia with an elevated urinary fractional excretion of potassium. Using a clearance technique, we detected higher fractional urinary potassium excretion in leptospirotic guinea pigs (26.5 +/- 4.7%) than in normal animals (14.1 +/- 2.8%, p < 0.05). After blocking distal NaCl reabsorption with furosemide, it was observed that in leptospirotic animals both fractional sodium excretion (40.0 +/- 7.4%) and fractional potassium excretion (136.3 +/- 32.7%) were higher than in normal animals (20.4 +/- 3.8%, p < 0.05, and 43.6 +/- 9.0%, p < 0.05, respectively). Microperfusion studies showed that the normal and leptospirotic medullary thick ascending limb had both identical transepithelial potential difference (+3.7 +/- 0.4 vs. 3.9 +/- 0.2 mV) and relative sodium-to-chloride permeability. The same technique showed that the osmotic water permeability (Posm; 0.9 +/- 0.4 x 10(-5) cm/s.atm) and diffusional permeability (34.7 +/- 6.6 x 10(-5) cm/s) observed in the leptospirotic inner medullary collecting duct (IMCD) in the presence of vasopressin were unchanged, as was also the case for urea permeability (3.74 +/- 0.7 x 10(-5) cm/s). These data show that acute renal failure in leptospirosis is characterized by tubular changes leading to potassium secretion probably due to a decrease in proximal sodium reabsorption. Furthermore, the inability to concentrate urine evidenced by the low P(o)sm present in leptospirotic animals is due, at least in part, to IMCD resistance to vasopressin.
Nephron 1992
PMID:Renal involvement in leptospirosis: a pathophysiologic study. 143 48

The role of hypothalamic paraventricular adrenoceptors and angiotensin II (ANG II)-AT 1 receptors in mediating the vasopressin (AVP) release into the plasma in response to i.c.v. and local paraventricular ANG II injections was investigated in conscious chronically instrumented rats. Noradrenaline (NA) administered bilaterally into the paraventricular nucleus (PVN) dose-dependently stimulated AVP release. Bilateral PVN microinjections of the alpha 1 adrenoceptor agonists methoxamine and phenylephrine, or of the alpha2 adrenoceptor agonist clonidine, did not affect plasma AVP when given alone, but increased plasma AVP when methoxamine and clonidine were given in combination. In contrast, PVN microinjections of both the beta 1 adrenoceptor agonist dobutamine and the beta 2 adrenoceptor agonist salbutamol significantly reduced basal plasma AVP. Bilateral PVN pretreatment with the alpha 1 and alpha 2 adrenergic antagonists prazosin, idazoxan and rauwolscine, but not of the beta 1 and beta 2 adrenoceptor antagonists atenolol and ICI 118 551, significantly attenuated the i.c.v. ANG II-induced AVP release. ANG II injected bilaterally into the PVN dose-dependently increased plasma AVP. Bilateral PVN pretreatment with the specific ANG II-AT 1 receptor antagonist losartan partially inhibited the i.c.v. ANG II-induced AVP release. We conclude: 1) Beta 1 and beta 2 adrenoceptors in the PVN exert an inhibitory action on basal AVP secretion. 2) ANG II can release AVP by directly stimulating its ANG II-AT 1 receptors in the PVN. 3) PVN mediated AVP release in response to periventricular ANG II-AT 1 receptor stimulation is at least partially effected through ANG II-AT 1 receptors in the PVN impinging on alpha adrenergic terminals.
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PMID:Involvement of adrenergic and angiotensinergic receptors in the paraventricular nucleus in the angiotensin II-induced vasopressin release. 146 31

The kidney consists of numerous functional units called nephrons. Thus, the use of individual nephron segments is essential to characterize their functional properties and to clarify the molecular basis of site-specific functions. Nephron segments can be microdissected from collagenase-treated renal slices under a stereomicroscope. A variety of intracellular ionic concentrations or membrane potential can be determined with various fluorescent probes. Fura-2/AM-loaded nephron segments reveal a transient increase of cytosolic free calcium concentrations by agonists such as angiotensin II, vasopressin, kinins, etc. To localize their receptors or to characterize their subtypes, this technique is especially beneficial, because tiny fragments of the nephron are sufficient by combination with a two-wave length microscope fluorometer. As an example, discovery of a novel vasopressin receptor (Vp) is described.
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PMID:[Usefulness of microdissection of nephron segments and fluorescent indicator for molecular biological studies of nephron functions]. 149 43

The noradrenergic innervation of vasopressin (VP)-containing neurons in the supraoptic nucleus (SON) of the rat hypothalamus was studied electron microscopically by using double-labeling immunocytochemistry combining the pre-embedding peroxidase-anti-peroxidase method with post-embedding immunocolloidal gold staining. Noradrenaline-like immunoreactive axon terminals were found to make synaptic contacts with neurophysin II-like immunoreactive neurons in the SON. This provides morphological evidence for noradrenergic control of neuronal activity of VP-containing neurons at the SON level.
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PMID:Noradrenergic innervation of vasopressin-containing neurons in the rat hypothalamic supraoptic nucleus. 150 81

It is well established that muscarinic cholinergic receptors are linked to phosphoinositide hydrolysis in brain. Previous studies of muscarinic responses used Li+ to increase inositol phosphate accumulation and suggested little or no change during aging. Li+ disrupts certain aspects of the inositol phosphate metabolism and inhibits the formation of inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. Ins(1,3,4,5)P4 appears to have second messenger functions. To investigate the effects of aging on agonist stimulated Ins(1,3,4,5)P4 formation, young (6-8 months) and old (28-30 months) Fischer 344 rat cerebral cortical or hippocampal slices were challenged with various agonists known to stimulate phosphoinositide hydrolysis in brain using a recently developed assay that does not use Li+. Carbachol and quisqualate stimulated [3H]inositol trisphosphate ([3H]InsP3) and [3H]Ins(1,3,4,5)P4 formation in young and old rat cerebral cortical slices. Norepinephrine, 5-hydroxytryptamine, and vasopressin failed to stimulate [3H]Ins(1,3,4,5)P4 or [3H]InsP3 formation in either young or old rat cerebral cortical slices. In old rat cerebral cortical slices, the carbachol-stimulated [3H]Ins(1,3,4,5)P4 formation was reduced by 44%. Angiotensin II stimulated [3H]InsP3 was increased (219%) in old rats. There was no influence of aging either on the basal level or on the maximal response to carbachol or quisqualate in hippocampal slices. These studies suggest region-specific changes in phosphoinositide hydrolysis during aging.
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PMID:Decreased carbachol-stimulated inositol 1,3,4,5-tetrakisphosphate formation in senescent rat cerebral cortical slices. 150 2

Atrial stretch and paracrine hormones stimulate atrial natriuretic peptide (ANP) secretion. The potential interplay between atrial stretch and paracrine hormones was examined. Isolated superfused rat left atria paced at 4 Hz were used for study. The effects of 0, 0.5, and 1.5 g settings of initial tension on the ANP secretory response to 1 microM norepinephrine and 10 nM endothelin were examined. The peak ANP secretory responses expressed as a percent of baseline for each of the tension settings were 109 +/- 8, 132 +/- 6, and 171 +/- 10% for norepinephrine and 285 +/- 15, 294 +/- 12, and 368 +/- 19 for endothelin, respectively. The effects of 0.5 microM norepinephrine, 1 nM endothelin, and 100 nM vasopressin on stretch-stimulated secretion were examined. Norepinephrine and endothelin increased ANP secretion 144 +/- 16 and 136 +/- 2% above baseline, respectively. Vasopressin did not increase ANP secretion. Norepinephrine and vasopressin did not significantly influence the ANP secretory response to stretch. In contrast, endothelin increased the response to stretch by 33% (P less than 0.035). We conclude 1) the greater the degree of atrial stretch, the greater is the response to norepinephrine and endothelin; 2) endothelin enhances the secretory response to stretch; and 3) norepinephrine and vasopressin do not affect stretch-stimulated release. These results predict a greater ANP secretory response to hormonal stimulation in vivo in volume-expanded states.
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PMID:Interaction between stretch and hormonally stimulated atrial natriuretic peptide secretion. 153 Nov 4

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.
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PMID:Widespread alterations in central noradrenaline, dopamine, and serotonin systems in the Brattleboro rat not related to the local absence of vasopressin. 169 74


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