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)

It was shown that kallikreinogen content was decreased in blood of old rabbits, kallikrein activity was somewhat increased, kininase activity was significantly decreased. In old animals, adenosine metabolism was activated, this being evident from the rise of 5'-nucleotidase and adenosine deaminase activity in blood and myocardium. Hypothalamic stimulation resulted in significant activation of the kallikrein-kinin system and sharp increase of kallikrein activity, the shifts being less marked in old animals than in adults. In adult animals, vasopressin administration elicited more marked activation of the kallikrein-kinin and adenosine metabolism systems.
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PMID:Kallikrein-kinin system and adenosine metabolism system of blood and heart and their changes at hypothalamic-hypophyseal stimulation in rabbits of different age. 624 32

Three structurally different drugs, MK421, SA446 and captopril, are angiotensin converting enzyme inhibitors. They induced a significantly greater fall in systolic blood pressure in sodium depleted rats than in sodium repleted ones. The combined administration of vasopressin or norepinephrine with MK421 eliminated the hypertensive effect of vasopressin or norepinephrine. Urinary kallikrein and kinin excretion were increased by MK421, SA446 or captopril in the sodium depleted rats whereas any significant changes in them were not observed in the sodium repleted rats. The combined administration of norepinephrine with MK421 induced further increases in urinary kallikrein and kinin excretion when compared to rats infused with norepinephrine alone, whereas the combined administration of vasopressin with MK421 did not induce any changes in them when compared to rats infused with vasopressin alone. Chronic infusion of captopril for up to 6 days in the rats induced a reduction of the vascular response to exogenous bradykinin; the blood pressure fall was less than that of the controls by 17% on Day 2 and by 18% on Day 6. These results indicate that the hypotensive response to angiotensin converting enzyme inhibitors was in part associated with the enhanced renal and vascular smooth muscle kallikrein-kinin system.
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PMID:Responses of the kallikrein-kinin system to angiotensin converting enzyme inhibitors in the rat. 632 15

Binding of intrinsically labeled [3H]bradykinin was studied in isolated nephron segments of the rabbit. Highest binding was observed in the cortical collecting tubule (5.76 +/- 0.34 X 10(-18) mol/mm) and the outer medullary collecting tubule (5.24 +/- 0.25 X 10(-18) mol/mm, means +/- SE, n = 6). Small but significant binding was also seen in the glomerulus, proximal straight tubule, cortical thick ascending limb of Henle's loop, and distal convoluted tubule. Lysyl-bradykinin, methionyl-lysyl-bradykinin, and tyrosine-8-bradykinin (but not des-arginine-9-bradykinin, vasopressin, angiotensins I and II, or prostaglandins) competed with [3H]bradykinin. The site of highest kinin binding (collecting tubule) is downstream from the highest concentration of kallikrein (granular portion of distal convoluted tubule). The binding data indicate that the major sites of kinin action in the kidney are the cortical and medullary collecting tubules. One action of kinins could be the stimulation of prostaglandin synthesis in the collecting tubules, which are known to actively synthesize prostaglandins.
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PMID:Binding of [3H]bradykinin in isolated nephron segments of the rabbit. 632 16

To study the hypotensive mechanism of the new oral converting-enzyme inhibitor, MK-421, we evaluated the antihypertensive effect of MK-421 in rats with hypertension induced by chronic administration of norepinephrine (NE) or vasopressin and measured urinary kallikrein and kinin excretions as indices of the renal kallikrein-kinin system. When 6 mg/kg/day of MK-421 was administered simultaneously with 1.8 mg/kg/day of NE, the systolic blood pressure of conscious rats rose on Day 1 to only 122.6 +/- 3.4 mm Hg compared with the rise to 146.3 +/- 1.6 mm Hg when NE alone was infused (p less than 0.001). Similarly, when the same dose of MK-421 was administered simultaneously with 7.2 U/kg/day of vasopressin, the systolic blood pressure of conscious rats rose on Day 1 to only 117.4 +/- 3.8 mm Hg compared with the rise to 141.6 +/- 3.4 mm Hg when vasopressin alone was infused (p less than 0.01). The antihypertensive effect of MK-421 was sustained for 6 days in rats infused with NE or vasopressin. Infusion of NE alone resulted in a small but significant increase in urinary kallikrein excretion and no change in urinary kinin excretion. The combined administration of NE with MK-421 induced additional increases in urinary kallikrein and kinin excretions. Vasopressin alone resulted in marked decreases in urinary kallikrein and kinin excretions. The combined administration of vasopressin with MK-421 induced no additional changes in urinary kallikrein and kinin excretion. These results indicate that the hypotensive effect of MK-421 may depend on a reduced sensitivity of the peripheral arteries to vasoconstrictor substances.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antihypertensive effect of MK-421 in rats. Role of the renal kallikrein-kinin system. 632 17

To study the relationship between vasopressin and the renal kallikrein-kinin system we measured the rate of excretion of kinins into the urine of anesthetized rats during conditions of increased and decreased vasopressin level. The excretion of immunoreactive kinins in Brattleboro rats with hereditary diabetes insipidus (DI) (24 +/- 3 pg min-1 kg-1) was lower than in the control Long Evans (LE) rats (182 +/- 22 pg min-1 kg-1; P less than 0.05). The DI rats also exhibited negligible urinary excretion of immunoreactive vasopressin, reduced urine osmolality, and increased urine flow and kininogenase excretion. In LE rats, volume expansion by infusion of 0.45% NaCl-2.5% dextrose to lower vasopressin secretion reduced (P less than 0.05) kinin excretion, vasopressin excretion, and urine osmolality to 41, 26, and 15% of their respective control values, while increasing (P less than 0.05) urine flow and kininogenase excretion. On the other hand, the infusion of 5% NaCl, which promotes vasopressin secretion, increased (P less than 0.05) the urinary excretion of kinins and vasopressin to 165 and 396% of control, while increasing (P less than 0.05) urine flow and kininogenase excretion. Infusion of vasopressin (1.2 mU/h, intravenous) enhanced (P less than 0.05) kinin excretion by two to threefold in DI rats and in LE rats during volume expansion with 0.45% NaCl-2.5% dextrose, while decreasing urine flow and increasing urine osmolality. This study demonstrates that the urinary excretion of immunoreactive kinins varies in relation to the urinary level of vasopressin, irrespective of urine volume and osmolality and of the urinary excretions of sodium and kininogenase. The study suggests a role for vasopressin in promoting the activity of the renal kallikrein-kinin system in the rat.
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PMID:Role of vasopressin in regulation of renal kinin excretion in Long-Evans and diabetes insipidus rats. 656 Dec 1

The urinary kallikrein system was studied during hyponatremia associated with water and vasopressin administration in rats. Two groups of animals were studied. In the experimental group (n = 5), vasopressin (0.4 U/day) was injected intramuscularly for 7 days, and water (15%-20% body weight per day) was given via a stomach tube. The control group (n = 6) received only vasopressin. In the experimental group, plasma sodium concentration (PNa) decreased from 143.2 +/- 0.5 to 130.8 +/- 1.8 (m +/- SEM) mmol/liter (5th day, p less than 0.01) along with plasma osmolality. Urinary kallikrein-like activities (UkaV) increased from 99.1 +/- 7.5 to 172.6 +/- 23.5 mumol X min/day (100 g body weight) (5th day, p less than 0.05; 6th day, p less than 0.05; and 7th day, p less than 0.05) after the administration of vasopressin. Uric acid clearance (Cua) increased from 0.153 +/- 0.014 to 0.275 +/- 0.041 ml/min (5th day, p less than 0.05; 7th day, p less than 0.05). No change was observed in urinary aldosterone excretion (UAldV), creatinine clearance, or blood pressure. UkaV correlated with Cua (r = 0.81, p less than 0.01) and with the degree of change of PNa (r = --0.79, p less than 0.01), respectively. In the control group, no change was observed in the above parameters. A significant relationship between UkaV and fractional Na clearance (r = 0.60, p less than 0.01) was observed. We conclude that the urinary kallikrein system in rats may be stimulated during hyponatremia when induced by water and vasopressin. This increased activity is probably the result of volume expansion associated with water and vasopressin and may have some relationship to fractional Na clearance in the kidney.
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PMID:Increased urinary kallikrein-like activity during ADH-induced hyponatremia in rats. 656 81

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.
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PMID:Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats. 656 34

In male Wistar rats, under osmotic diuresis, the effect of angiotensin II, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion were evaluated. Angiotensin II did not modify but all the others drugs used increased significantly the urinary kallikrein excretion. In all the groups studied the urinary sodium excretion increased. No modifications were observed in urine flow, glomerular filtration rate, urine osmolality and potassium excretion. The urinary kallikrein excretion was always positively correlated with the urinary flow and urinary sodium excretion. No correlation was observed with the other parameters studied. These findings suggest that noradrenaline, vasopressin and aldosterone are important stimulators of the urinary kallikrein excretion. Probably, kallikrein is one of the mechanisms involved in the regulation of urinary sodium excretion.
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PMID:Effect of angiotensin, noradrenaline, vasopressin and aldosterone on urinary kallikrein excretion in the rat. 656 41

In an attempt to investigate a possible interaction between vasopressin and the renal kallikrein-kinin system, renal function and urinary kallikrein excretion were monitored in trained conscious dogs and in anesthetized rats in water diuresis and in vasopressin-induced antidiuresis. Vasopressin elevated urinary kallikrein excretion in a dose-dependent way in both species, with concomitant increases in urinary osmolality and electrolyte excretion. A significant increase in kallikrein excretion was observed with a dose of vasopressin as low as 2 mU . kg-1 . h-1 in the dog and 3 mU . kg-1 . h-1 in the rat without a change in renal hemodynamics. In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. It is concluded that vasopressin over its normal physiological range of concentration stimulates renal kallikrein secretion.
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PMID:Effect of vasopressin on renal kallikrein excretion. 690 27

The present experiments were performed to investigate whether the responses of the myoepithelium to several drugs would be of a parallel nature with those of the vascular smooth muscle in the lactating mammary gland of goats. The drugs were injected into the mammary artery. Kallikrein, bradykinin, oxytocin, and acetylcholine caused marked milk-ejection with vasodilation in a dose-dependent manner. Marked milk-ejections with high doses of oxytocin were observed despite of accompanying vasoconstriction. The relative order of their potency in milk-ejection activity was kallikrein greater than bradykinin greater than oxytocin greater than acetylcholine: 1 greater than 1/100 greater than 3/1000 greater than 5/1000000. As for the vasodilator activity, the relative potency of the drugs was in the same order: 1 greater than 1/10 greater than 1/1000 greater than 1/10000. Catecholamines, histamine, serotonin, angiotensin-II, vasopressin and high doses of prostaglandin E2 caused dose-dependent vasoconstriction. Isoprenaline, pilocarpine, adenosine, PGI2 and low doses of PGE2 caused dose-dependent vasodilation. But these drugs did not affect milk-ejection. PGE1 decreased milk-ejection and was accompanied by vasodilation. From these experiments it is suggested that the relative order of the potency of secretagogues in milk-ejection activity and in vasodilator activity is nearly equal. It is also suggested that some drugs are different in their effects on the myoepithelium and on the vascular smooth muscle of the lactating mammary gland.
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PMID:Pharmacological effects of several drugs on the myoepithelium and the vascular smooth muscle of the lactating mammary gland in goats. 692 Feb 63


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