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PubMed1995

Bladder mast cell expression of high affinity oestrogen receptors in patients with interstitial cystitis.

OBJECTIVE: To investigate the role of oestrogens in the pathophysiology of interstitial cystitis (IC), specifically with respect to activated bladder mast cells (MC), as well as urine concentrations of MC-derived histamine and methylhistamine, all of which are increased in patients with IC. This goal appeared important because IC is a bladder disorder which occurs almost exclusively in women, and is characterized by polyuria, nocturia and pelvic pain, which worsen perimenstrually. PATIENTS AND METHODS: Biopsies from six patients with IC and four control patients were analysed blindly for the presence of oestrogen receptors (OR) using both custom-made and commercially available antibodies against OR. RESULTS: Bladder MC alone were shown to express high-affinity OR and there was a higher number of such cells present in patients with IC compared with controls. The identity of MC in the bladder was documented with immunohistochemistry for tryptase. OR were also identified in human MC (HMC-1), a MC line kept in culture. These steps were necessary because of the unique finding that only MC express OR, in spite of the inflammatory infiltrate present. CONCLUSION: These findings may help to explain why IC occurs primarily in women, why IC and other associated symptoms tend to be worst at the midcycle, and may also suggest that prognostic usefulness of staining bladder biopsies for OR. These results are particularly interesting because oestradiol has been shown to augment MC histamine secretion in response to the neuropeptide, substance P, which may be released in certain neuroinflammatory disorders which have a high prevalence in women, such as IC and irritable bowel syndrome.

Cystitis↗
PubMed2004

Antidiuretic hormone in elderly male patients with severe nocturia: a circadian study.

OBJECTIVE: To investigate the circadian variation of plasma antidiuretic hormone (ADH) and urine output in patients with severe nocturia (> three times per night) and to assess the effect of oral desmopressin on nocturnal urine output in these patients. PATIENTS AND METHODS: Twelve patients with severe nocturia and five age-matched controls without were assessed over 24 h (circadian sampling) during a 72-h hospital admission. Blood levels of ADH and changes of urine output were measured in the patients before and after the oral administration of desmopressin (0.2 mg, at 22.00 hours in the second day), and in the controls not treated with desmopressin. RESULTS: Compared with the normal control, the patients had no diurnal variation in urine output and greater nocturnal urine production, associated with a lack of nocturnal increase in ADH level. Compared with the baseline urine output, desmopressin significantly decreased night-time (23.00-08.00 hour) urine output in the patients (P < 0.05). Desmopressin significantly increased the osmolality of night-time urine (P < 0.05), and there was no systemic adverse reaction. CONCLUSIONS: Severe nocturia in a large proportion of elderly men with lower urinary tract symptoms is caused by nocturnal polyuria and natriuresis, because they have no nocturnal increase in ADH. These results suggest that desmopressin may be effective in decreasing nocturnal urine production in patients with severe nocturia who do not respond to conventional treatment.

Aged↗
PubMed1991

Public awareness of the symptoms of diabetes mellitus.

A cross-sectional survey by standard questionnaire was conducted to determine the public's knowledge (n = 480) of diabetes and diabetes symptoms. Four hundred and sixty-two (96%) subjects had heard of diabetes, 350 (73%) could give a rudimentary definition of diabetes, but 231 (48%) were unable to name any symptom and only 20 (4%) knew of thirst and polyuria in combination. The public's knowledge of diabetes symptoms is poor. This may possibly contribute to delayed presentation of Type 2 diabetes.

Adult↗
PubMed1992

Clinical and laboratory features of type 1 diabetic children at the time of diagnosis.

The French incidence study has registered all new cases of Type 1 diabetic children under 20 years of age, from a population of 2.32 million, in an exhaustive and prospective manner. Three hundred and forty cases were identified between 1 January 1988 and 31 December 1989, yielding a mean annual incidence rate 7.3 per 10(5). The lowest rate was observed in the youngest age group (0-4 yr: 4.1 per 10(5)) and the highest around pubertal development (10-14 yr: 11.5 per 10(5)). Details of the previous personal and family history, and the clinical and biological pictures of the disease at diagnosis were recorded. Almost 8 per cent of the children had a first-degree relative with Type 1 diabetes. Polyuria, weight loss, fatigue and abdominal pain were the most frequently reported symptoms, which were of median duration 4.4 months. Mean weight loss before diagnosis was 9.4 +/- 6.8 (+/- SD)% of body weight and was not significantly related to age. Ketonuria was detected in 83.8 per cent and acidosis (total CO2 less than or equal to 18 mmol l-1, if measured) in 48 per cent of the cases. Ketonuria and acidosis were significantly more frequent in the younger age group than in the rest of the group (p less than 0.001).

Adolescent↗
PubMed2000

Role of water channels in fluid transport studied by phenotype analysis of aquaporin knockout mice.

Aquaporin-type water channels are expressed widely in mammalian tissues, particularly in the kidney, lung, eye and gastrointestinal tract. To define the role of aquaporins in organ physiology, we have generated and analysed transgenic mice lacking aquaporins (AQP) 1, 3, 4 and 5. Multiple phenotype abnormalities were found in the null mice. For example, in kidney, deletion of AQP1 or AQP3 produced marked polyuria whereas AQP4 deletion produced only a mild concentrating defect. Deletion of AQP5, the apical membrane water channel in the salivary gland, caused defective saliva production. Deletion of AQP1 or AQP5, water channels in lung endothelia and epithelia, resulted in a 90% decrease in airspace-capillary water permeability. In the brain, deletion of AQP4 conferred marked protection from brain swelling induced by acute water intoxication and ischaemic stroke. The general paradigm that has emerged from these phenotype studies is that aquaporins facilitate rapid near-isosmolar transepithelial fluid absorption/secretion, as well as rapid vectorial water movement driven by osmotic gradients. However, we have found many examples in which the tissue-specific expression of an aquaporin is not associated with any apparent phenotypic abnormality. The physiological data on aquaporin null mice suggest the utility of aquaporin blockers and aquaporin gene replacement in selected human diseases.

Animals↗
PubMed1988

Glucose transporter of the blood-brain barrier and brain in chronic hyperglycemia.

The effect of chronic hyperglycemia on the glucose transporter moiety of the blood-brain barrier and cerebral cortex was studied in rats 3 weeks after the administration of a single intravenous dose of streptozotocin (60 mg/kg), using specific [3H]cytochalasin B binding methods. Streptozotocin-treated rats developed hyperglycemia, as well as polydipsia and polyuria, and failed to gain weight. The density of D-glucose-displaceable cytochalasin B binding sites in the brain microvessels of streptozotocin-treated hyperglycemic rats was increased by about 30% compared with those of control rats, without change in the affinity of binding. Chronic hyperglycemia had no effect on the density or affinity of specific binding of cytochalasin B to cerebral cortical membranes. These findings do not support the hypothesis that glucose transporters in brain microvessels comprising the blood-brain barrier are "down-regulated" in chronic hyperglycemia.

Animals↗
PubMed1987

Effects of extracellular fluid volume changes on renal response to low-dose dopamine infusion in normal women.

Dopamine (DA) i.v. infused in a low dose (0.1 microgram/kg/min) in healthy women during sustained hypotonic polyuria, produced different renal functional effects as variations in extracellular fluid volume occurred. (1) In hydro-saline retention (n = 23), induced by desoxycorticosterone acetate treatment, DA produced typical vasodilator and hydro-natriuretic effects (Goldberg, 1972). (2) In hydro-saline depletion (n = 19), induced by diuretic treatment and low dietary sodium intake, DA lost its vasodilator and natriuretic efficacy, manifesting, on the other hand, renal sodium conserving effects mainly dependent on the increase in distal sodium reabsorption and a trend towards afferent arteriolar vasoconstriction. (3) Treatment with prazosin (n = 9) or propranolol (n = 9) in hydro-saline depletion, was efficacious in partly restoring the typical vasodilator and natriuretic effects of DA. Thus, in hydro-saline depletion, DA produced sympathomimetic effects which were sufficiently intense to outweigh those due to activation of specific DA renal receptors.

Adult↗
PubMed1994

Effects of angiotensin-converting enzyme inhibition on renal dysfunction induced by moderate potassium depletion in healthy women.

The role of the renin-angiotensin system in renal hypokalaemic dysfunction has been investigated by evaluating the effects of the angiotensin (AT)-converting enzyme inhibition by enalapril. Healthy women were studied either in normal potassium balance (N3, n = 6) or moderate potassium depletion (KD3, n = 6). Potassium depletion (KD) was induced by low potassium dietary intake (greater than or equal to 10 mmol per day) and natriuretic treatment associated with replacement of net NaCl and water losses; the cumulative potassium deficit achieved was 214 +/- 54 mmol. The renal function and the urinary excretions of some prostanoids (PGE2, 6-keto-PGF1 alpha, TxB2) were evaluated during hypotonic polyuria (oral water load) and subsequent moderate antidiuresis (lysine-8-vasopressin (LVP) low-dose infusion). Paired studies were performed in absence (control) and presence of enalapril. Basal plasma renin activity (PRA) and urinary aldosterone excretion were determined before the water load of control studies. Renal dysfunction typical of chronic KD occurred in the KD3 group, i.e. increase in PRA, decrease in creatinine clearance, depression of the diuretic response to water load, inhibition of distal fractional chloride reabsorption, and blunted efficacy of LVP in increasing the urinary solute concentration. The urinary prostanoid excretions were reduced. Basal urinary aldosterone excretion was not changed significantly. In KD3 group enalapril decreased mean arterial pressure (MAP), increased the plasma potassium concentration, improved the diuretic response to water load and corrected the impairment of the distal fractional chloride reabsorption. Despite the decrease in MAP enalapril did not affect significantly the creatinine clearance. Neither urinary prostanoid excretions nor the renal response to LVP were affected by the drug. The data suggest that in KD the increased activity of the renin-angiotensin system affected the renal function both through direct effects and through effects dependent on the angiotensin-supported secretions of aldosterone and probably of vasopressin. Finally, by comparing the effects of enalapril and indomethacin in experimental groups with an equivalent degree of KD, evidence is provided in favour of the interaction between renin-angiotensin and prostanoid systems in controlling the glomerular filtration rate and the salt and water handling by renal tubules.

Adult↗
PubMed1974

The effect of chlorpropamide on water balance in pitressin-treated Brattleboro rats.

1 The daily administration of a 5% glucose solution to the heterozygous Brattleboro rat produced an experimental model in a comparable state of polydipsia and polyuria to the homozygous rat with diabetes insipidus (DI).2 The effect of chlorpropamide on water metabolism was then examined in both the homozygous DI rat treated with submaximal doses of pitressin tannate in oil (Pitressin), and in the glucose-hydrated heterozygous rat with and without simultaneous pitressin therapy.3 A dose-response curve for chlorpropamide (5, 10, and 20 mg/24 h) in DI rats treated with Pitressin (25 mu/24 h) indicated that the drug decreased fluid intake further, but only by a maximum of 13.8% (at the 20 mg/24 h dose of chlorpropamide), differing markedly from results obtained in patients with diabetes insipidus. A second experiment in which chlorpropamide (5 mg/24 h) was administered to DI rats treated with Pitressin (either 25 or 50 mu/24 h) confirmed the lack of any significant drug-effect on water metabolism in these animals.4 Chlorpropamide (20 mg/24 h), when administered alone or simultaneously with a submaximal dose of Pitressin (25 mu/24 h), had no obvious effect on the fluid intake of glucose-hydrated heterozygous rats. The absence of any action by chlorpropamide on water metabolism was confirmed in these experimental animals using 5 mg/24 h of the drug together with Pitressin (either 25 or 50 mu/24 hours).5 Indirect evidence for the slower growth-rate in the DI rat being due to an insufficient daily calorific intake was obtained from the study on glucose-hydrated heterozygous rats.

Analysis of Variance↗
PubMed1977

Time course of lithium-induced alterations in renal and endocrine function in normal and Brattleboro rats with hypothalamic diabetes insipidus.

1. A lithium chloride (1.1 g/kg) supplemented diet was given to Long Evans (LE) and Brattleboro (DI) rats to investigate its actions in the presence (LE) and absence (DI) of vasopressin. 2. During the first 24 h, Li-supplemented LE rats displayed an initial water deficit (drinking less than renal output), increased plasma antidiuretic (ADH) titres and slightly increased plasma renin activities (PRA) and plasma osmolarities. Such changes were qualitatively similar to those seen in rats fed a normal diet, but deprived of water for 24 hours. After 12 days, the Li-supplemented rats had elevated plasma ADH titres, but reduced pituitary oxytocic and antidiuretic activities. 3. The urinary losses of Na, K and Cl exceeded dietary intakes in LE rats on the introduction of the Li-supplement, and the urinary osmolarity fell by 50%. Electrolyte balances were gradually re-established, although drinking and urine production increased in parallel to reach twice the control values by day 12 of the supplement. 4. Aldosterone and corticosterone secretory rates and their peripheral plasma concentrations were unchanged both after 24 h and 28 days of the Li-supplement. 5. Li elicited no water deficit or saluresis in DI rats, and although the polyuria and polydipsia were exacerbated, urinary osmolarity did not change over the 12 day observation period. 6. Li increased Ca excretion in both rat types; after 12 days the PRA of DI but not LE animals were increased. 7. It is concluded that the overall renal actions of Li are tempered by vasopressin rather than adrenocorticosteroids.

Adrenal Cortex↗
PubMed1984

Naloxone reduces diuretic responses induced by water, alcohol or congenital lack of vasopressin in rats.

The effects of naloxone (2 and 10 mg kg-1 s.c.) were compared in several kinds of experimental polyuria: alcohol- or water-loaded rats and Brattleboro rats (i.e. animals with congenital lack of vasopressin). In normal rats, both water and alcohol increased urine flow and decreased urinary osmolality. Alcohol induced a more marked diuretic response than water. In normally hydrated rats, naloxone (2 and 10 mg kg-1 s.c.) failed to modify urine flow, urinary osmolality, Na+ and K+ urinary excretion, and urine creatinine concentration. The two doses of naloxone decreased urine flow and increased osmolality in both water- and alcohol-loaded rats. In Brattleboro rats, naloxone (10 mg kg-1 s.c.) reduced urine flow and urinary creatine whereas the low dose (2 mg kg-1 s.c.) was without effect. Since it is well known that the mechanism of water- or alcohol-induced diuresis is an inhibition of vasopressin release, the present results suggest that naloxone could prevent this inhibition. They indicate that endogenous opioid peptides may exert an inhibitory control on vasopressin release.

Animals↗
PubMed2004

Homozygosity for uromodulin disorders: FJHN and MCKD-type 2.

BACKGROUND: Autosomal-dominant medullary cystic kidney disease type 2 (MCKD2) and familial juvenile hyperuricemic nephropathy (FJHN) are heritable renal diseases with autosomal-dominant transmission and shared features, including polyuria, progressive renal failure, and abnormal urate handling, which leads to hyperuricemia and gout. Mutations of the UMOD gene, disrupting the tertiary structure of uromodulin, cause MCKD2 and FJHN. METHODS: Haplotype analysis of a large Spanish family with MCKD was carried out to determinate genetic linkage to MCKD2 locus. Mutation detection was performed by direct sequencing of the UMOD gene. The level of Tamm-Horsfall protein in the urine was measured by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot analysis. RESULTS: Linkage to MCKD2 locus was demonstrated (LOD score: 4.13), and a known pathogenic uromodulin mutation was found in exon 4, corresponding to Cys255Tyr, disrupting the light chain binding domain of the protein. In this consanguineous family there were three patients homozygous for the C255Y mutation, and multiple heterozygous cases, allowing the MCKD phenotypes associated with one or two mutant alleles to be compared. The homozygous individuals survived to adulthood, although presenting an earlier onset of hyperuricemia and faster progression to end-stage renal disease than heterozygous individuals. Western analysis revealed lower levels of urine THP in one heterozygous patient compared with a normal control patient, both with normal renal function. CONCLUSION: The study shows that individuals with two UMOD mutations are viable, but they do have more severe disease on average than heterozygotes. This family sheds light on the possible disease mechanism in this disorder.

Adult↗
PubMed2005

Vasopressin-independent regulation of collecting duct aquaporin-2 in food deprivation.

BACKGROUND: Humans and animals are frequently subjected to food deprivation or starvation. However, the adaptation of the kidney to this condition is not well understood. The purpose of these studies was to examine the effects of food deprivation on water handling by the kidney, the expression levels of collecting duct (CD) water channel aquaporin-2 (AQP2), and to determine the role of vasopressin in the adaptation of AQP2 to food deprivation. METHODS: Sprague-Dawley (SD) and Brattleboro rats were placed in metabolic cages and deprived of food but had free access to water for 72 hours. Water balance and urine osmolality were measured daily. Kidney tissues were isolated and examined for the expression of AQP2 using semiquantitative immunoblotting and Northern hybridization. The circulating level of vasopressin and the mRNA expression levels of its precursor were determined by radioimmunoassay and Northern hybridization, respectively. RESULTS: In SD rats, the first 24 hours of food deprivation is associated with a significant polyuria and decreased urine osmolality (Uosm). This correlated with a significant down-regulation of AQP2 in the cortex and outer medulla. After 72 hours of food deprivation, Uosm increased above baseline, and urine volume dropped to a lower value. This was associated with a rebound increase in AQP2 expression in the cortex and OM and its up-regulation in the inner medulla. Interestingly, vasopressin mRNA expression and plasma levels were unchanged during food deprivation. Further, in homozygous Brattleboro rats, in which endogenous vasopressin is absent, food deprivation caused changes in urine volume, urine osmolality, and AQP2 expression, which are qualitatively similar to those observed in normal rats. CONCLUSION: Food deprivation impairs water handling by the kidney by causing dual changes in urine volume and urine osmolality. This effect is associated with parallel alterations in the expression of AQP2 and is independent of vasopressin activity. It is concluded that the increase in water reabsorption in the CD is an adaptive response of the kidney to a long period of food deprivation and is mediated via a vasopressin-independent mechanism.

Adrenal Cortex Hormones↗
PubMed2005

Effects of renin-angiotensin system blockade on renal angiotensin-(1-7) forming enzymes and receptors.

BACKGROUND: Angiotensin-converting enzyme (ACE)2, a homologue of ACE, which is insensitive to ACE inhibitors and forms angiotensin-(1-7) [Ang-(1-7)] from angiotensin II (Ang II) with high efficiency was investigated in response to chronic blockade with lisinopril, losartan, and both drugs combined. METHODS: Thirty-six adult Lewis rats were assigned to receive these medications in their drinking water for 2 weeks while their arterial pressure, water intake, and urine volume were recorded throughout the study. Measures of renal excretory variables included assessing excretion rates of angiotensin I (Ang I), Ang II and Ang-(1-7) while blood collected at the completion of the study was used for measures of plasma angiotensin concentrations. Samples from renal cortex were assayed for renin, angiotensinogen (Aogen), neprilysin, angiotensin types 1 and 2 (AT(1) and AT(2)) and mas receptor mRNAs by semiquantitative reverse transcriptase (RT) real-time polymerase chain reaction (PCR). ACE2 activity was determined as the rate of Ang II conversion into Ang-(1-7). RESULTS: Comparable blood pressure reductions were obtained in rats medicated with either lisinopril or losartan, whereas both drugs produced a greater decrease in arterial pressure. Polyuria was recorded in all three forms of treatment associated with reduced osmolality but no changes in creatinine excretion. Lisinopril augmented plasma levels and urinary excretion rates of Ang I and Ang-(1-7), while plasma Ang II was reduced with no effect on urinary Ang II. Losartan produced similar changes in plasma and urinary Ang-(1-7) but increased plasma Ang II without changing urinary Ang II excretion. Combination therapy mimicked the effects obtained with lisinopril on plasma and urinary Ang I and Ang-(1-7) levels. Renal cortex Aogen mRNA increased in rats medicated with either lisinopril or the combination, whereas all three treatments produced a robust increase in renal renin mRNA. In contrast, ACE, ACE2, neprilysin, AT(1), and mas receptor mRNAs remained unchanged with all three treatments. Renal cortex ACE2 activity was significantly augmented in rats medicated with lisinopril or losartan but not changed in those given the combination. CONCLUSION: Our data revealed a role for ACE2 in Ang-(1-7) formation from Ang II in the kidney of normotensive rats as primarily reflected by the increased ACE2 activity measured in renal membranes from the kidney of rats given either lisinopril or losartan. The data further indicate that increased levels of Ang-(1-7) in the urine of animals after ACE inhibition or AT(1) receptor blockade reflect an intrarenal formation of the heptapeptide.

Angiotensin I↗
PubMed2005

Polycystic kidney disease.

Polycystic kidney disease, an inherited systemic disorder, is characterized by the development of multiple cysts in the kidneys and other organs. Patients can present at any age, but more often come to clinical attention (unless there is a family history) after age 30. Patients who are diagnosed before age 30 have a worse renal survival. Although palpation of the abdomen occasionally provides a clue to the presence of polycystic kidney disease, radiographic procedures most often suggest the diagnosis. Mutations in the PKD1 or PKD2 genes give rise to cyst formation. Flank pain, hematuria, polyuria, nephrolithiasis, urinary tract infections, and hypertension may be part of the syndrome of polycystic kidney disease. It is the fourth most common cause of end-stage renal disease. Blood pressure treatment goals are less than 130/80 mm Hg. Treatment should include the use of angiotensin-converting enzyme inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Migraine symptoms: results of a survey of self-reported migraineurs.

Migraine is an episodic headache disorder associated with various combinations of neurologic, gastrointestinal, and autonomic symptoms. Gastrointestinal disturbances including nausea, vomiting, abdominal cramps, or diarrhea are almost universal. Sensory hyperexcitability manifested by photophobia, phonophobia, and osmophobia are frequently experienced. Other symptoms include blurry vision, nasal stuffiness, tenesmus, polyuria, pallor, and sweating. Our telephone interview survey of 500 self-reported migraine sufferers was performed in 1994. The most common reported symptoms associated with migraine were pain, nausea, problems with vision, and vomiting. Nausea occurred in more than 90% of all migraineurs; nearly one third of these experienced nausea during every attack. Vomiting occurred in almost 70% of all migraineurs; nearly one third of these vomited in the majority of attacks. In those who experienced nausea, 30.5% indicated that it interfered with their ability to take their oral migraine medication; in those with vomiting, 42.2% indicated that it interfered with their ability to take their oral migraine medication. The most important features of a migraine medication were rapid and effective relief of headache pain, decreasing the likelihood of headache recurrence, and not causing nausea. Many migraine patients suffer needlessly because their nausea and vomiting are both unreported to, and unrecognized by physicians. The presence of these symptoms is crucial to diagnose migraine not accompanied by aura.

Acute Disease↗
PubMed1998

Arginine vasopressin levels in nursing home residents with nighttime urinary incontinence.

OBJECTIVES: To examine the relationship between diurnal urine volume and plasma arginine vasopressin levels (AVP) in nursing home residents with nighttime urinary incontinence and a comparison group of frail but nondemented, continent geriatric board and care residents. DESIGN: Case series. SETTING: Four nursing homes and two board and care facilities. PARTICIPANTS: Sixty-two nursing home residents and 27 board and care residents. MEASUREMENTS: Daytime (7:00 a.m. to 7:00 p.m.) and nighttime (7:00 p.m. to 7:00 a.m.) urine volumes of incontinent nursing home residents were measured over 3 days and 3 nights by reweighing preweighed adults diapers and toileting inserts emptied by research staff for the comparison group. AVP levels were drawn in the early morning (5:00 a.m. to 7:00 a.m.) before subjects arose and in the evening after an hour of lying in bed (8:00 p.m. to 11:00 p.m.), and plasma levels were determined by radioimmunoassay. RESULTS: Half of the nursing home residents and 82% of the comparison group had night/total urine volume ratios > or = 50%. Forty-nine percent of the total of 89 subjects had undetectable morning AVP levels, 61% had undetectable evening AVP levels, and 42% had undetectable AVP levels in both morning and evening. There were no significant differences in AVP levels between those with night/total urine volume ratios > or = 50% and < 50% in either the nursing home or comparison groups though the small number of comparison group subjects with ratios < 50% may have limited our statistical power to detect differences. CONCLUSION: Our data suggest that a substantial proportion of both nursing home residents with nighttime incontinence and frail geriatric patients with a reversal of the normal diurnal pattern of urine excretion have an accompanying deficiency in AVP production and/or secretion. More detailed physiologic studies are needed to understand better the pathophysiology of geriatric nocturia and nighttime incontinence and the role that AVP deficiency may play in these conditions. Until such studies are carried out, we do not recommend the routine use of exogenous AVP for geriatric patients with unexplained nocturnal polyuria.

Aged↗
PubMed1997

Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia.

Thirty-two consecutive patients with paroxysmal supraventricular tachycardias, with previously defined mechanisms of the tachycardias, were interviewed by noninvestigators about whether they experienced symptoms of diuresis during or at the termination of the tachycardias, to test the hypothesis that patients with AV nodal reentrant tachycardia would have a feeling of diuresis, polyuria, or both during or at the termination of the tachycardia. Twelve of the 13 patients with AV nodal reentrant tachycardia (92%), two of the 15 patients with AV reentrant tachycardia (13%), and one of the 4 patients with atrial flutter associated with 2:1 AV conduction (25%) felt diuresis during or at the termination of the tachycardias (AV nodal reentrant tachycardia vs other forms of tachycardia; P < 0.001). In 14 of the 32 patients, the right atrial pressure and plasma atrial natriuretic peptide (ANP) concentration were measured during both the tachycardias and sinus rhythm. The mean right atrial pressure during AV nodal reentrant tachycardia was significantly elevated compared to that during other forms of tachycardia (P < 0.01). The plasma ANP concentration during AV nodal reentrant tachycardia was also elevated significantly compared to that during other forms of tachycardias (P < 0.001). There were no significant differences in the cycle lengths of the tachycardias, age, left atrial dimensions, or the left ventricular ejection fraction between the AV nodal reentrant tachycardia and the other forms of tachycardia. We concluded that the feeling of diuresis during or at the termination of tachycardia was a more common symptom in patients with AV nodal reentrant tachycardia. The higher secretion of plasma ANP from the right atrium might be involved in the mechanism of this symptom.

Atrial Natriuretic Factor↗