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 vasoconstrictors angiotensin II, vasopressin and the alpha-sympathomimetic phenylephrine significantly inhibit the renin release caused by the beta-sympathomimetic isoprenaline. The mechanism of the inhibition is discussed.
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PMID:Inhibition of isoprenaline-induced increase in plasma renin concentration by vasoconstrictors. 117 48

The effect of i.v. infused (asp1-beta-amid, val5)-angiotensin II (1.0 mug/kg min), octapressin (phe2, lys8-vasopressin) (10.0 mU/kg min) and of the alpha-sympathomimetic amine phenylephrine (40.0 mug/kg min) on the stimulation of renin secretion by furosemide (10.0 mg/kg i.v.) was investigated. The vasoconstrictors abolished the renin release induced by forosemide. Studies on the clearance of p-aminohippuric acid (PAH) (i.e. renal plasma flow) showed that the action of the vasoconstrictors cannot be explained by a decrease in access of furosemide to its intrarenal sites of action. The mechanism of the suppressive action of the vasoconstrictors on renin release is discussed.
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PMID:Inhibition of furosemide-induced renin release by vasoconstrictors. 118 24

The purpose of this study was to determine whether centrally administered renin stimulated vasopressin secretion. Vasopressin was not measured directly, but, instead, changes in urinary water excretion in anesthesized dogs undergoing a water excretion in anesthetized dogs undergoing a water diuresis were used as an index of changes in vasopressin secretion. Intraventricular injection of hog renin in a dose of 0.1 Goldblatt unit produced a marked decrease in urine flow which was associated with a decrease in free water clearance and an increase in urinary osmolatiy with no change in osmolar clearance. Sodium excretion increased significantly but there was no change in potassium excretion. These effects, which closely resemble those resulting from an increase in vasopressin secretion, were prevented by hypophysectomy. The antidiuretic effect clearly resulted from an action of renin in the central nervous system since renin had no effect on urine flow or osmolality when administered intravenously. Intraventricular administration of saralasin acetate, a specific antagonist of angiotensin II, completely blocked the effects of intraventricular renin indicating that these effects were mediated via the formation of angiotensin II. The data therefore indicate that there is an interaction between injected renin, brain angiotensinogen, and converting enzyme resulting in the formation of angiotensin II which stimulates the secretion of vasopressin. Additional studies are required to determine whether the brain renin-angiotensin system plays a physiological role in the regulation of a vasopressin secretion.
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PMID:Antidiuresis produced by injection of renin into the third cerebral ventricle of the dog. 124 51

To investigate the interaction between antidiuretic hormone (ADH) and renin-angiotensin system, plasma ADH and plasma renin activity (PRA) were determined in normal subjects (n = 10) under various hydrated states. Four experimental conditions, i.e., water loading, infusion of hypertonic saline, acute dehydration induced by furosemide and postural changes, were chosen. 1. Upright posture decreased plasma volume by 9.5 +/- 0.9% without significant changes in plasma osmolality. PRA increased from 5.2 +/- 0.7 to 8.3 +/- 0.8 ng/ml. However, plasma ADH did not change significantly (1.9 +/- 0.3 to 1.8 +/- 0.2 muU/ml). 2. When furosemide was administered intravenously under this condition, both plasma ADH and PRA increased to 3.1 +/- 0.5 muU/ml and 15.5 +/- 1.6 ng/ml with 11.2 +/- 1.1% decrease in plasma volume. Plasma osmolality did not change significantly. 3.Water load resulted in a decrease in plasma osmolality from 282.6 +/- 0.9 to 278.6 +/- 1.2 mOsm/kg without significant change in plasma volume. Significant decrease in plasma ADH level from 2.6 "/- 0.4 to 0.6 "/- 0.1 muU/ml was found, but PRA (7.8 +/- 1.1 ng/ml) did not change (6.3 +/- 1.0 ng/ml). 4. Hypertonic saline infusion brought about an increase in plasma osmolality to 290.1 +/- 0.8 mOsm/kg with simultaneous increase in plasma volume by 6.7 +/- 1.3%. Plasma ADH level also increased to 2.4 +/- 0.3 muU/ml, while PRA decreased to 4.2 +/- 0.3 mg/nl. Accordingly, significant correlation between changes in PRA and plasma ADH level, was not observed. We suggest that plasma osmolality is the dominant variable in regulating plasma ADH level, but in the presence of a sufficient degree of hypovolemia, the osmotic domination was overcome. On the other hand, PRA was strongly influenced by changes in effective blood volume other than changes in plasma osmolality.
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PMID:Effect of various states of hydration on plasma ADH and renin in man. 124 95

The effect of acute administration of 2 preparations of growth hormone (hGH) on plasma renin activity (PRA) was studied in normal volunteers. 4 IU of standard, commercially available hGH II, Kabi, Sweden) were injected im into each of four normal subjects, and the PRA was determined in the basal state and at 30, 60, 120, 180, and 240 min after injection. Free fatty acid (FFA) was determined basally and at 15 and 210 min post-injection. The study was repeated on a different day in the same group using highly purified hGH (hGH I, 4 IU) virtually free of arginine-vasopressin. Four other normal subjects received 12 IU standard hGH (hGH II, Kabi, Sweden). There was no significant difference in PRA values with 4 IU of either preparation or with 12 IU of hGH II in any of the groups, although mean PRA was elevated in two of the patients receiving 12 IU hGH II. A rise in FFA occurred in all subjects, indicating the biological activity of hGH preparations. The possible significance of these findings to the renin-angiotensin system found in acromegaly is considered.
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PMID:The effect of different preparations of human growth hormone on plasma renin activity in normal males. 126 36

The effects of dopamine on plasma renin-angiotensin-aldosterone system vasopressin levels and blood pressure were studied in anesthetized guinea-pig. The inhibition of the angiotensin converting enzyme with perindopril permitted assessment of the role of the renin-angiotensin system. In perindopril-treated guinea-pigs, the activity of angiotensin-converting enzyme was decreased by 90% with simultaneous increases in plasma renin activity and angiotensin I concentration; aldosterone and vasopressin levels, blood pressure and heart rate were not modified. Dopamine depressed mean arterial pressure by 30% and increased heart rate (8%) in controls. Dopamine infusion did not affect either plasma renin activity or angiotensin I concentration or angiotensin-converting enzyme activity in control animals. But in perindopril pretreated animals it further increased plasma renin activity (88%) and angiotensin I concentration (35%). Finally, in controls, dopamine infusion increased plasma vasopressin concentrations (91%) whereas this increase did not occur in perindopril treated animals.
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PMID:Endocrine and hemodynamic responses to dopamine infusion in the guinea-pig: effects of ACE inhibition with perindopril. 128 86

The cause of hyponatremia following subarachnoid hemorrhage (SAH) has been understood as an inappropriate secretion of antidiuretic hormone (SIADH). Whereas, water restriction for the management of this condition sometimes induces a severe dehydration, resulting in vasospasm. To clarify the pathogenesis of hyponatremia following SAH, we measured the daily sodium and water balance with the plasma concentration of atrial natriuretic peptide (ANP), antidiuretic hormone (ADH), and plasma renin activity (PRA) in seventeen cases after subarachnoid hemorrhage. Although the patients received an adequate amount of fluid (more than 4080ml/day; daily average in seventeen cases) and sodium (more than 277 mEq/day; daily average in seventeen cases), eight out of the seventeen cases showed transient hyponatremia of a slight degree beginning on 8.8 days after SAH. ANP values were elevated markedly in fifteen out of the seventeen cases, remaining high during the first two weeks following SAH. ADH values were elevated remarkably in eight out of the seventeen cases. However, these values declined immediately to a normal range within two days following SAH. PRA were increased or came within the normal range, suggesting the lack of water retention. Overall sodium balance and water balance did not differ significantly between hyponatremia cases and normonatremia ones, whereas, sodium balance in acute phase was significantly negative, associated with marked natriuresis in patients with hyponatremia. These correlations suggested that hyponatremia after SAH is the result of natriuresis by an increased ANP rather than ADH. In conclusion, a greater replenishment of water and sodium is required to avoid hyponatremia with dehydration. This technique may be helpful for the prevention of vasospasms following SAH.
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PMID:[Pathogenesis of hyponatremia observed in the treatment of acute subarachnoid hemorrhage]. 128 91

We examined the acute effects of bilateral subdiaphragmatic vagotomy (BSV) on blood pressure and renal function in female Sprague-Dawley rats. Mean arterial pressure was greater (p < 0.0001) in rats with BSV than in sham-operated rats (SOR). Rats with BSV had a significantly lower effective renal plasma flow (p < 0.01), total sodium excretion (p < 0.005), fractional sodium excretion (p < 0.01), urine flow (p < 0.01), and fractional excretion of water (p < 0.02) than SOR. The glomerular filtration rate was not significantly different between the 2 groups of rats. Plasma potassium was greater in rats with BSV than in SOR (p < 0.02). Pretreatment with an inhibitor of the angiotensin-converting enzyme prevented the above changes in rats with BSV. Changes in renal function and mean arterial pressure could not be attributed to antidiuretic hormone since plasma levels of antidiuretic hormone were lower in rats with BSV than in SOR (p < 0.002). In addition, the activity of the sympathetic system was decreased in rats with BSV, as suggested by the lower plasma levels of epinephrine (p < 0.003) and norepinephrine (p < 0.02) and the significantly lower renal tissue concentrations of norepinephrine (p < 0.03). No significant changes in renal tissue concentrations of acetylcholine or choline, its precursor, were observed in BSV rats when compared to SOR, suggesting a lack of renal parasympathetic innervation. Plasma renin activity was lower in rats with BSV (p < 0.02) than in SOR, but this effect was blunted in rats given an angiotensin-converting enzyme inhibitor prior to BSV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Subdiaphragmatic vagotomy in rats induces systemic hypertension and sodium retention. 129 60

During a 25-day space mission of French cosmonaut on board Mir station, the joint Soviet-French Czecho-Slovak experiment "Minilab" has been conducted in order to evaluate a fluid-electrolyte metabolism status and its hormonal control at different flight stages and early postflight. In cosmonaut venous blood was drawn twice, and 24-hour urine samples were collected on mission Days 5 and 19. With the aid of Plasma-02 equipment the blood plasma and urinary samples were treated, frozen and maintained aboard the station. Postflight, frozen samples were delivered to the laboratory for further analyses. In-flight, urinary excretion of fluid and sodium decreased by 25-35%. On mission Day 9, the blood plasma levels of vasopressin increased by 450% and on Day 20 by 700% as opposed to the baseline levels, blood aldosterone content was also elevated with an increased renal excretion of both hormones. Blood plasma renin activity elevated two-fold, and atrio-natriuretic factor (ANF) content practically did not differ from a baseline value. In-flight circulating plasma volume (CPV) decreased by 20%. Postflight, there occurred the body hypohydration and activation of the hormonal systems providing a retention of body fluids and electrolytes to restore an adequate CPV and fluid-electrolyte homeostatic as a whole.
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PMID:[Water-salt metabolism and its hormonal regulation studied in the 2nd joint Soviet-French space flight]. 129 42

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).
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PMID:[Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]. 130 Feb 58


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