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)

A rise in cytosolic free calcium ([Ca2+]i) is thought to be the principal mediator in vascular smooth muscle contraction. Quantitative changes of [Ca2+]i in response to two vasoconstrictor peptide hormones, angiotensin II and vasopressin, were directly measured in monolayers of adherent cultured rat aortic smooth muscle cells loaded with the fluorescent calcium indicator Quin 2. Angiotensin II induced rapid, concentration-dependent rises in [Ca2+]i from 1.53 +/- 0.27 X 10(-7) (n = 16) up to 1.2 X 10(-6) M, with ED50 of 0.45 X 10(-9) M, an effect which was blocked by the antagonist analogue [Sar1, Ala8]angiotensin II. Vasopressin also elicited transient rises in [Ca2+]i to peak levels of about 8 X 10(-7) M, with ED50 of 1.05 X 10(-9) M, and this response was completely abolished by a vasopressor antagonist. In calcium-free medium, basal [Ca2+]i levels fell to 0.92 +/- 0.24 X 10(-7) M (n = 4), and both hormones were still able to raise [Ca2+]i, although to a lesser extent. Readdition of extracellular calcium following the [Ca2+]i transient induced a second, slower [Ca2+]i rise. In calcium-containing medium, lanthanum ion (2 X 10(-5) M) reduced peptide-evoked [Ca2+]i rises to the values observed in calcium-free medium. Stimulation with each peptide completely desensitized the smooth muscle cells to a subsequent identical challenge, with little crosstachyphylaxis. Potassium ion (50 mM) only minimally affected [Ca2+]i levels. The calcium channel blocker nifedipine (10(-6) M) did not prevent the [Ca2+]i rises induced by angiotensin II, vasopressin, or potassium. These findings indicate that the two physiologically important vasoconstrictor hormones angiotensin II and vasopressin rapidly raise [Ca2+]i in cultured vascular smooth muscle cells, in part by mobilizing calcium from intracellular pools and in part through activation of receptor-operated calcium channels.
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PMID:Cytosolic free calcium levels in monolayers of cultured rat aortic smooth muscle cells. Effects of angiotensin II and vasopressin. 400 79

Acute hypercalcemia in the conscious, unanesthetized rat, achieved by a 30-minute infusion of CaCl2 (serum calcium level, 12.8 +/- 0.6 mg/dl) resulted in significant elevation of mean arterial pressure (from 112 +/- 2 mm Hg to 129 +/- 3 mm Hg, p less than 0.001). This pressor response was associated with a significant increase in systemic vascular resistance, from 0.45 +/- 0.02 mm Hg/(ml/min)/kg body weight to 0.50 +/- 0.02 mm Hg/(ml/min)/kg body weight (p less than 0.05), but it caused no alteration in cardiac index. The pressor response to acute hypercalcemia does not appear to be mediated by vasopressor hormones or attenuated by vasodepressor hormones since inhibition of the renin-angiotensin system (nephrectomy), catecholamines (central and peripheral 6-hydroxydopamine), vasopressin (vascular antagonist), prostaglandins (indomethacin), and parathyroid hormone (parathyroidectomy) did not significantly alter the pressor response to infusion of CaCl2 in spite of similar serum calcium levels in all groups of animals. Rather, the pressor response to acute hypercalcemia seems to be mediated by a direct action of calcium ion on smooth muscle and perhaps myocardial cell contractility, since pretreatment with the calcium channel blockers verapamil or nifedipine blocked the pressor response to acute hypercalcemia.
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PMID:Mechanism of acute hypercalcemic hypertension in the conscious rat. 407 24

Prostacyclin (PGI2) and prostaglandin E2 (PGE2) production by rat glomerular epithelial cells in culture were stimulated by arginine vasopressin (AVP) over a dose range of 10(-9) to 10(-6) M, but only if the cells were allowed to recover from trypsin treatment. The effect of AVP was related to its pressor activity since the antidiuretic analogue of AVP, 1-deamino-8-D-Arg-vasopressin (dDAVP) had no effect. Angiotensin II and kallidin (lysyl-bradykinin) did not affect prostaglandin production by these cells. The stimulatory effect of AVP on arachidonate metabolism was inhibited by the calcium channel antagonist, nifedipine, in a dose-dependent fashion suggesting that cellular uptake of calcium was required.
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PMID:Stimulation of prostaglandin production in rat glomerular epithelial cells by antidiuretic hormone. 608 84

The effects of vanadate on cardiovascular function and on the secretion of renin and vasopressin were investigated by infusing sodium orthovanadate (0.32 mu mole/kg X min) intravenously into five conscious dogs. Vanadate caused significant increases in mean arterial pressure, total peripheral resistance, pulmonary arterial pressure, and cardiac output. These data illustrate that the hemodynamic effects of vanadate in the conscious dog are similar to those of the anesthetized dog but that minor differences do exist. Vanadate significantly suppressed plasma renin activity, but plasma vasopressin was unchanged. The effects of vanadate also were investigated in the same dogs on another day after administration of the calcium channel blocker, verapamil (0.3 mg/kg bolus + 0.01 mg/kg X min). After calcium channel blockade, the increases in arterial pressure and pulmonary arterial pressure induced by vanadate were attenuated, and cardiac output did not increase. Calcium channel blockade also prevented the vanadate-induced decrease in plasma renin activity. These data suggest that the cardiovascular and humoral alterations produced by vanadate in the conscious dog are at least partially mediated by changes in intracellular calcium.
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PMID:Cardiovascular and renin responses to vanadate in the conscious dog: attenuation after calcium channel blockade. 636 50

Historically, the sodium ion has been given prominence in relation to cardiovascular disease, perhaps to the exclusion of other ions. Recently, other ions, including chloride, potassium, magnesium and calcium have received increasing attention in relation to hypertension, cardiac arrhythmias, and metabolic derangements. Endocrine factors controlling these ions have also received increasing attention; they include classic hormonal actions as well as neurotransmission and paracrine hormonal actions. Studies indicate that control of the renin-angiotensin-aldosterone system resides in cytosolic calcium ion levels in the juxtaglomerular cell, as well as chloride ion and prostaglandins at the macula densa. Renin release is stimulated by hyperpolarisation of the juxtaglomerular cell induced by beta 1-agonists, parathyroid hormone, glucagon, magnesium and low cytosol calcium. Renin release is inhibited by high calcium, potassium and angiotensin II. Subsequent to renin release, hormonal regulation includes stimulation of converting enzyme activity by cortisol and prostaglandin (PGE2). Other hormonal control includes antidiuretic hormone producing dilution of extracellular electrolytes and augmented peripheral resistance. A recently identified natriuretic factor isolated from cardiac atria appears to be a potent diuretic with actions similar to that of frusemide (furosemide). Other electrolytes have received closer scrutiny. Chloride may play a dominant role in renal sodium reabsorption, responding to prostaglandin levels. Calcium has been recognised as a basic regulator of the secretion of such hormones as noradrenaline, renin, and aldosterone. As well, calcium ion changes are the means by which smooth muscle contraction is effected. Parathyroid hormone and vitamin D regulate the level of this ion in the body. In addition, a high dietary calcium intake appears to play a protective role against hypertension, while calcium channel blockers appear to reduce blood pressure. Endocrine systems play a major role in the protection against acute elevations in serum potassium by means of insulin action and adrenergic modulation of extrarenal potassium disposal. Aldosterone is recognised as the delayed regulator of potassium excretion. Magnesium levels fall in hyperaldosteronism, hyperparathyroidism, and diabetic keto-acidosis, as well as in malnutrition states. A coexisting potassium deficiency may be refractory to therapy until hypomagnesaemia is corrected. The integrated action of these hormones and electrolytes are thus of major importance in regulation of the cardiovascular system.
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PMID:Endocrine physiology of electrolyte metabolism. 638 78

The noncontractile aortic cell line A7r5 was chosen to study the effect of the vasoconstrictor peptide vasopressin on transmembrane Ca2+ movements, using conventional whole-cell patch recording techniques. Conditions in which previously characterised vasoconstrictor-modulated currents were suppressed revealed a tiny inward current component (-18 +/- 2 pA, n = 50, at -61 mV in 110 mM CaCl2). The vasopressin-activated inward current was absent when Ca2+ was absent from the extracellular solution, and the current amplitude increased with [Ca2+] (0.01-110 mM), with an apparent dissociation constant for Ca2+ of 9.7 mM. It was highly selective for Ca2+ over monovalent cations (permeability ratio Ca/Cs greater than 17). It was not voltage gated, except that the current/potential characteristic showed some inwards rectification. Amplitudes of the evoked inward currents had the same order of magnitude in Sr2+ and Ca2+, whereas they were much smaller in Mn2+, suggesting that this pathway is highly permeable to Sr2+ but poorly permeable to Mn2+. Inward currents evoked in Ca2+ were inhibited by other cations with the following order of potency: La3+ > Cd2+ > Co2+ approximately Ni2+ approximately Mn2+. The channel producing this current corresponds most probably to the ionic pathway originally called the receptor-operated calcium channel, which produces a long-lasting, constrictor-induced plateau of increased intracellular free calcium concentration in smooth muscle.
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PMID:Identification of the Ca2+ current activated by vasoconstrictors in vascular smooth muscle cells. 770 69

The influx of calcium in response to vasopressin receptor stimulation is an important component of excitation-contraction coupling. We have examined the routes by which Ca2+ and other divalent cations enter vascular smooth muscle cells using a cultured vascular smooth muscle cell line (A7r5). Confluent A7r5 cells were loaded with Fura-2 to permit measurement of intracellular divalent cation concentration (Ca2+, Ba2+, Mn2+). Combinations of excitation wavelengths (340/380, 340/356, 356/380 and 340/370) were used depending on the divalent cation being studied. Emission was measured at 510 nm for all studies. Ca2+, Ba2+ and Mn2+ permeated unstimulated A7r5 cells. Vasopressin increased intracellular Ca2+ in cells both in the presence and absence of extracellular Ca2+, although responses in the absence of extracellular Ca2+ were smaller and had no sustained component. Amlodipine, a voltage-dependent calcium channel blocker, had no effect on Ca2+ entry, but Ni2+ did block Ca2+ influx. Vasopressin-induced elevations of intracellular Ca2+ in Ca(2+)-free physiological saline were abolished by ionomycin and thapsigargin. In the presence of extracellular Ba2+ vasopressin increased intracellular Ca2+ transiently and caused a small sustained increase in intracellular Ba2+ concentration. Ionomycin and thapsigargin increased intracellular Ca2+ but had no effect on Ba2+ influx. In contrast vasopressin, ionomycin and thapsigargin had no effect on Mn2+ influx. Econazole and SKF 96365, imidazoles reported to be blockers of receptor-induced cation entry, increased intracellular Ca2+ by releasing intracellular Ca2+ from a different site to that mobilized by vasopressin or thapsigargin in A7r5 cells. Econazole and SKF 96365 partially inhibited passive influx of Ca2+ and Ba2+ but did not inhibit passive influx of Mn2+, or vasopressin-induced influx of Ba2+. U73122, a putative inhibitor of phospholipase C partially inhibited passive entry of Ca2+ but not passive entry of Mn2+ and Ba2+. U73122 also inhibited vasopressin-induced release of intracellular Ca2+ and agonist-induced Ca2+ influx but did not block vasopressin-induced Ba2+ influx. Divalent cations enter A7r5 cells by a number of routes - 'passive' pathway(s) that admit Ca2+, Ba2+ and Mn2+ and receptor-operated pathway(s) that are permeable to Ca2+, Ba2+ but not Mn2+. On the basis of ionic permeabilities and the effect of various blocking agents, there appear to be two distinct passive influx routes. One is permeable to Ca2+ and Ba2+ and is blocked by econazole or SKF 96365. The other is permeable to Mn2+ and is blocked by Ni2+. There also appear to be two different routes of divalent cation entry involved in responses to receptor activation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multiple pathways for entry of calcium and other divalent cations in a vascular smooth muscle cell line (A7r5). 805 48

The effects of a calcium channel blocker, nicardipine, on pressure-natriuresis responses were studied in Dahl salt sensitive (DS) and resistant (DR) rats. Differences in the neural and endocrine background were minimized by renal denervation and by holding plasma vasopressin, aldosterone, corticosterone, and norepinephrine levels constant by intravenous infusion. The renal plasma flow (RPF) and glomerular filtration rate (GFR) of DS rats were disautoregulated in the low renal perfusion pressure range, while those of DR rats were autoregulated. Administration of nicardipine (0.3 microgram/kg/min) into the renal artery significantly increased RPF and GFR and abolished the autoregulation in both strains of rats. Nicardipine also sharpened the pressure-natriuresis responses in both strains without changes in fractional excretion of sodium. These findings suggest that nicardipine increased GFR and thereby improved the pressure-natriuresis responses of DS rats.
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PMID:Effects of a calcium channel blocker, nicardipine, on pressure-natriuresis in Dahl salt-sensitive rats. 813 77

The effects of a combination of vasopressin and a calcium channel blocker (nicardipine) on portohepatic hemodynamics and liver function were compared with the effects of vasopressin alone in 18 patients with portal hypertension. Nine patients received 0.4 units/min of vasopressin and 9 patients received the same dose of vasopressin plus 0.3 mg/min of nicardipine for 40 min. Vasopressin plus nicardipine induced a significant reduction in both free portal venous pressure and the portal venous pressure gradient. These effects were similar to the changes with vasopressin alone (-14% vs. -16% in free portal venous pressure; -29% vs. -31% in portal venous pressure gradient). Vasopressin decreased both hepatic blood flow (-34%, P < 0.01) and intrinsic clearance of indocyanine green (-22%, P < 0.05). In contrast, these two parameters did not significantly change after vasopressin plus nicardipine (-8% and -3%, respectively). These results suggest that the addition of nicardipine improves hepatic impairment induced by vasopressin but causes no further reduction on portal pressure.
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PMID:Effects of vasopressin and nicardipine on hemodynamics and liver function in patients with cirrhosis: comparison with vasopressin alone. 815 Oct 95

This overview summarizes the major and minor side effects and drug interactions of fluoxetine. The adverse reactions include the "serotonin syndrome", cardiovascular complications, extrapyramidal side effects such as akathisia, dyskinesias, and parkinsonian-like syndromes and an apparently increased risk of suicidality. Fluoxetine-induced mania and hypomania, seizures and sexual disorders are evaluated along with minor symptoms of allergic reactions, stuttering, hematological changes, psoriasis, and inappropriate secretion of the antidiuretic hormone. The major fluoxetine-drug interactions involve the amino acids L-dopa and L-tryptophan, anorexiants, anticonvulsants, antidepressants, anxiolytics, calcium channel blockers, cyproheptadine, lithium salts, and drugs of abuse. The underlying mechanism and the paradoxical effects of fluoxetine are addressed.
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PMID:Fluoxetine: adverse effects and drug-drug interactions. 825 2


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