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 responsiveness of retinal vasculature to i.v. administration of several potent vasoactive agents was studied in pentobarbital anesthetized rats by taking fundus photographs. Since cerebral vasculature had been claimed to react in a similar manner but less liably than retinal vessels to some vasoactive substances, the findings were applied to the problem of reactivity of brain vessels. Sublethal doses of noradrenaline, adrenaline, 5-hydroxytryptamine, angiotensin amide and arginine orlysine vasopressin caused no marked acute ( less than or equal to 2 min) vasoconstriction in retinal vessels. Nor did any of these agents or bradykinin elicit vasodilatation. The late vasoconstriction (greater than 2 min) found in succumbing animals was most likely unspecific, since it did not occur until severe toxic symptoms appeared. The findings support the concept that intracerebral vessels are quite resistant to the direct action of many vasoactive agents given i.v.
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PMID:The poor reactivity of retinal vessels to systemic administration of vasoactive agents in pentobarbital anesthetized rats. 89 23

The effect of bradykinin on the renal medullary osmotic gradient was evaluated in anesthetized dogs which were undergoing water diuresis and which received a unilateral renal arterial infusion of bradykinin. The effect of the peptide on the medullary osmotic gradient was determined by analysis of medullary tissue electrolyte and urea concentrations and by analysis of changes in urine osmolality induced by vasopressin. Bradykinin decreased the total osmolality per kg H2O in tissue from inner medulla and papilla (-18.7 +/- 6% and -19.3 +/- 8%) and increased fractional water excretion (3.8 +/- 1.3%). Furthermore, a direct relationship between changes in free water clearance and changes in papillary tissue, osmolality was found. Finally, the increase in urine osmolality after ADH was significantly less in vasodilated than in control kidneys. These results indicate that bradykinin can diminish the medullary osmotic gradient during water diuresis in the dog. Thus, a bradykinin-induced increase in free water clearance may be accounted for by other than an inhibition of proximal tubular sodium reabsorption.
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PMID:Effect of bradykinin on the renal medullary osmotic gradient in water diuresis. 90 88

Spontaneous rhythmic activity, responses to drugs and effects of field stimulation of nerves of the retractor penis (rp) and/or corpus cavernosum urethrae (ccu) of macaque, rabbit, guinea-pig, rat, dog, cat, horse, boar, elk, bull, ram and goat, as well as of the penile artery (pa) of bull were studied. A basic property of all these muscles was automaticity. Their responses to 5-hydroxytryptamine, histamine, adenosine triphosphate, prostaglandins E1, E2, AND F2alpha, oxytocin, vasopressin, substance P, bradykinin and angiotensin exhibited considerable species variations. Their excitatory innervation seems to be adrenergic. They also have an inhibitory innervation. In spite of comprehensive pharmacological analysis the inhibitory mediator remains obscure. The frequency--response relationship to inhibitory nerve stimulation was characterized by a rapidly achieved maximum at low frequencies, indicating high efficiency of the neuroeffector unit.
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PMID:Comparative study of some isolated mammalian smooth muscle effectors of penile erection. 92 Feb 6

Contractile responses of isolated dog veins to bradykinin were studied. Responses to norepinephrine were taken as standards. According to their sensitivity to bradykinin, the veins obtained from 14 sites of the venous system were divided into two groups, while all the veins were almost uniform in their sensitivity to norepinephrine. One group has high sensitivity to bradykinin and the other has low sensitivity. The former includes the pulmonary, hepatic, splenic, and portal veins, the anterior vena cava, and the upper and the middle divisions of the posterior vena cava. The latter includes the external jugular, cephalic, azygos, femoral, and saphenous veins, and the lower division of the posterior vena cava. The responses of the renal vein were intermediate. A striking correlation was noted between the distribution of bradykinin sensitivity and the genesis of the venous system. Five bioactive peptides other than bradykinin were also studied. Only angiotensin induced contraction in some preparation, but, as a whole, caerulein, eledoisin-related peptide, oxytocin and vasopressin rarely showed contractile activity.
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PMID:Responsiveness of isolated dog veins to bradykinin and other bioactive peptides: distribution of sensitivity to bradykinin and possible correlation with genesis of the venous system. 94 11

Maintenance of normotension rests upon the overall salt and water balance, which, in the event of disequilibrium, modifies body fluid, cardiac output and total peripheral resistance. The kidneys play a central role in this hydro-saline regulation. The central and autonomous nervous systems, the renin-angiotensin system, the mineralocorticoids, the antidiuretic hormone and the kallikrein-bradykinin-prostaglandin system all affect this regulation and are closely interrelated. The role of each of these nervous and endocrine systems in hypertension, and their close interrelationship, is briefly reviewed.
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PMID:[Physiopathology of arterial hypertension. Role of the nervous system and of the hormones]. 101

The superior mesenteric blood flow was studied with a dye-dilution technique after catheterization of the superior mesenteric artery and vein. The investigation was performed in connection with portography in 22 patients with apparently normal small bowel function. Intra-arterial injection of 5, 10 or 20 mug bradykinin was followed within one minute by an increase, on the average, of 114, 176 and 223% respectively, in the superior mesenteric blood flow. The blood flow was dose-dependent in this range. The estimated vascular resistance decreased by 52, 61 and 67%, respectively. The portal venous pressure was increased slightly after intra-arterial injection, but the pressure was unchanged after intra-portal injection. Intra-arterial injection of bradykinin causes a highly improved venous phase at superior mesenteric angiography. This may be due not only to the increased flow but to some extent also to increased capillary permeability produced by bradykinin. Intra-arterial injection of 0.125 and 0.250 IU of vasopressin decreased the superior mesenteric blood flow by 53 and 54%, respectively, within 3 minutes of the injection. The dye-dilution method used was not applicable to blood flow below a level of about 200 ml/min. Continuous infusion of 0.05 IU/min decreased the superior mesenteric blood flow by, on an average, 58%. The portal venous pressure was decreased by 25% after the intra-arterial injection, but no change in pressure was recorded after intra-portal administration. The clinical use of intra-arterial infusion of vasopressin during gastrointenstinal bleeding is discussed.
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PMID:Superior mesenteric blood flow in man following injection of bradykinin and vasopressin into the superior mesenteric artery. 109 45

Hemodynamic effects of the kallikrein-kinin system can be investigated by experimental administration of specific kinin antagonists and by measurement of kinin levels in the circulating blood. In conscious normal rats, the bradykinin analog B4162 blunts the hypotensive effect of exogenous bradykinin. This kinin antagonist has no blood pressure effect in control rats, but it enhances the pressor effect of vasoconstrictor substances such as vasopressin or angiotensin II when they are infused at subpressor doses. Endogenous kinins may therefore participate in blood pressure regulation by antagonizing pressor substances. Plasma levels of endogenous kinins are normally in the low picomolar range. They are rapidly generated and destroyed in biological fluids. Thus, measurement of plasma kinins requires sensitive assays based on high-affinity antibodies and careful sample-handling techniques. Nonpolar solid-phase extraction on phenylsilylsilica provides a rapid, reliable, and easy extraction of kinins from plasma with constant and high recoveries.
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PMID:Antagonizing and measurement: approaches to understanding of hemodynamic effects of kinins. 128 26

We evaluated whether the brain kallikrein-kinin system plays a role in the regulation of adrenocorticotropin (ACTH) release in rats. Intracerebroventricular (icv) injection of bradykinin (0.24 nmol) increased plasma immunoreactive ACTH (irACTH) levels (from 93 +/- 4 to 200 +/- 12 pg/ml, P less than 0.01). This effect was prevented by icv kinin antagonist at 15.4 nmol/h (from 98 +/- 5 to 108 +/- 6 pg/ml; not significant). The antagonist did not alter the increase in plasma irACTH levels induced by icv corticotropin-releasing factor (CRF), arginine vasopressin, or prostaglandin E2. Melittin (7 nmol/h icv) increased plasma irACTH from 95 +/- 4 to 268 +/- 7 pg/ml (P less than 0.01). This effect was prevented by icv kinin antagonist (15.4 nmol/h), kallikrein antibodies (13 pmol/h), or indomethacin (0.28 mmol/h). ACTH response to melittin was not altered by antagonists of CRF or vasopressin. Intra-arterial injection of insulin (0.3 IU/kg body wt) reduced plasma glucose levels to a similar extent in rats given icv kinin antagonist or vehicle; the ACTH response to insulin-induced hypoglycemia was slightly less in rats given kinin antagonist than in those given vehicle (55 +/- 5 vs. 86 +/- 4 pg/ml, P less than 0.05). The brain kallikrein-kinin system may play a role in the regulation of ACTH secretion in stimulated conditions.
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PMID:Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release. 131 88

The receptor agonist-mediated hydrolysis of phosphoinositides and production of prostacyclin were studied in murine cerebral endothelial cells (MCEC). Of 11 neurotransmitters and neuromodulators examined, carbachol, noradrenaline (NE), bradykinin, and thrombin significantly increased 3H-inositol phosphate accumulation in the presence of LiCl (20 mM). The maximal stimulation of [3H]inositol monophosphate ([3H]IP1) reached approximately 11, 11, seven, and four times the basal levels for carbachol, NE, bradykinin, and thrombin, respectively. The EC50 values of IP1 accumulation for carbachol and NE were 34 and 0.16 microM, respectively. The muscarinic antagonists, atropine and pirenzepine, blocked the carbachol-induced IP1 accumulation with Ki values of 0.3 and 30 nM, respectively. The adrenergic antagonist, prazosin, blocked NE-induced IP1 accumulation with a Ki of 0.1 nM. The calcium ionophore A23187, histamine, glutamate, vasopressin, serotonin, platelet activating factor, and substance P did not stimulate IP1 accumulation. A23187, bradykinin, and thrombin stimulated prostacyclin release to approximately four, four, and two times the basal levels, respectively, whereas carbachol and NE had little effect upon prostacyclin release. These results suggest that the activation of phospholipase C and of phospholipase A2 in MCEC are regulated separately.
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PMID:Receptor-linked hydrolysis of phosphoinositides and production of prostacyclin in cerebral endothelial cells. 131 55

Neuropeptides are increasingly implicated in the control of cell proliferation and their mechanisms of action are attracting intense interest. The early complex cascade of events initiated by peptides of the bombesin family including gastrin-releasing peptide is increasingly understood. The cause-effect relationships and temporal organization of these early signals and molecular events provide a paradigm for the study of other growth factors and mitogenic neuropeptides and illustrate the activation and interaction of a variety of signaling pathways. These peptides may also act as autocrine growth factors for certain small cell lung cancer cells. The results discussed here strongly suggest that the autocrine growth loop of bombesin-like peptides may be only a part of an extensive network of autocrine and paracrine interactions involving a variety of Ca(2+)-mobilizing neuropeptides in small cell lung cancer including bradykinin, cholecystokinin, galanin, neurotensin, and vasopressin. In this context, broad spectrum antagonists that prevent the function of multiple Ca(2+)-mobilizing receptors are of special interest. These antagonists block neuropeptide mediated signals and inhibit small cell lung cancer growth in vitro and in vivo. Thus, broad spectrum neuropeptide antagonists constitute potential anticancer agents.
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PMID:Growth of small cell lung cancer cells: stimulation by multiple neuropeptides and inhibition by broad spectrum antagonists in vitro and in vivo. 131 36


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