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PubMed1980

"Exaggerated" natriuresis in experimental hypertension and the role of the natriuretic factor.

In rabbits with experimental ischaemic cerebral hypertension the role of the natriuretic factor in the genesis of the phenomenon of "exaggerated" natriuresis after extracellular space expansion was studied. In control animals an expansion of the extracellular fluid was followed by an elevation of the natriuretic factor in blood, whereas in hypertensive rabbits the phenomenon did not appear. Besides, in hypertensive rabbits the urinary excretion and the clearance of the natriuretic factor were considerably higher than in the control animals. In the genesis of exaggerated natriuresis in hypertension a certain role is doubtlessly played by the natriuretic factor.

Animals↗
PubMed1994

Abnormal pressure-natriuresis in transgenic renin gene rats.

OBJECTIVE: Pressure-diuresis-natriuresis relationships were compared in rats made transgenic by implantation of the mouse salivary gland renin gene [TGR(mRen-2)27 rats] and Sprague-Dawley/Hannover rats to determine whether resetting of renal function contributes to the development of hypertension in these rats. METHODS: Differences in the neural and hormonal background were minimized by denervating the kidney and holding plasma vasopressin, aldosterone, cortisol and norepinephrine levels constant by intravenous infusion. RESULTS: In Hannover rats (n = 9), urine flow and sodium excretion increased from 26.4 +/- 6.2 to 86.8 +/- 8.6 microliters/min per g kidney weight and from 5.1 +/- 0.8 to 15.3 +/- 1.0 mumol/min per g kidney weight as renal perfusion pressure (RPP) was increased from 107 to 153 mmHg. The renal blood flow (RBF) and glomerular filtration rate (GFR) were well-autoregulated and averaged 6.6 and 1.5 ml/min per g kidney weight throughout the range of pressures studied. In TGR (n = 10), urine flow and sodium excretion increased from 30.0 +/- 6.1 to 59.7 +/- 7.2 microliters/min per g kidney weight and from 3.8 +/- 0.9 to 8.5 +/- 1.3 mumol/min per g kidney weight in response to an elevation in RPP from 170 to 212 mmHg. The RBF and GFR were about 20% lower in TGR than in Hannover rats and averaged 4.1 and 1.0 ml/min per g kidney weight, respectively. CONCLUSION: The results show that the pressure-diuresis-natriuresis relationship is shifted to higher pressure levels in TGR and that this is associated with enhanced tubular reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

[Taste receptor response to sodium chloride and natriuresis in the workers and employees of an industrial enterprise].

Studied in the course of one-stage epidemiologic survey of 1191 individuals were the threshold of gustatory sensitivity to table salt and nycterine natriuresis, relation of these indices to dietary habits, some risk factors for cardiovascular disorders and clinical parameters. Differing relations were established between gustatory sensitivity to table salt and natriuresis and age and gender of the examinees, the level of blood pressure, aggravated heredity in respect of arterial hypertension, smoking and alcohol abuse, this enabling one to embark upon a differential approach to dietetic correction of salt consumption.

Adult↗
PubMed1995

[Natriuresis and atrial natriuretic factors during extracorporeal circulation for cardiac surgery].

At the end of cardiopulmonary bypass (CPB) diuresis and natriuresis are widely modified. Those are classically due to the CPB conditions (mean arterial pressure, non pulsatile flow, hypothermia, long duration ...). Previous studies showed no evidence of these modifications being due to variations of hormones such as vasopressin, renin or aldosterone. The atrial natriuretic factor, cardiac hormone mainly known for its natriuretic effect, would contribute to explain these facts. This study includes 17 patients NYHA I or II without any renal dysfunction or diabetes mellitus. They were scheduled for cardiac surgery under CPB (valvular replacement or aortocoronary bypass). Sampling times were: TO: after induction of anaesthesia and before surgical incision; T1: during steady CPB; T2: 30 min after CPB release. At each time were obtained: diuresis, osmolar and free water clearance, fractional excretion of sodium, haematocrit, plasma concentration of ANF (pANF), and right atrial pressure and capillar wedge pressure in case of aortocoronary graft. FeNa at the end of CPB is significantly linked to the osmolar clearance and the CPB duration. FeNa evolution is parallel with pFAN evolution. At the end of CPB pFAN is first linked to cardiac rate, then to CPB duration. Cardiac filling pressures after and before CPB are not different. pANF after CPB cannot be attributed to these pressures. Numerous factors are involved in the renal sodium elimination. An evident statistic link between pANF and FeNa is then difficult to demonstrate. Their parallel evolution is coherent and suggests that ANF is the main hormone of natriuresis at the end of CPB. ANF secretion factors at the end of CPB remain unclear. This study emphasizes the involvement of cardiac rate and CPB duration in pANF increase at the end of CPB.

Adult↗
PubMed1996

Chronic effects of nitric oxide and prostaglandin inhibition on pressure diuresis and natriuresis in rats.

The long-term interaction between nitric oxide (NO) and prostaglandins (PGs) in the pressure diuresis and natriuresis response has been studied. Experiments were performed in rats with chronic (8 weeks) inhibition of NO (NG-nitro L-arginine methyl Ester, L-NAME, 40 mg/kg/day) with or without simultaneous PGs synthesis blockade (indomethacin, 1 mg/kg/day). A time control group with no treatment was studied in parallel. At the end of this period, the animals were anesthetized and renal hemodynamics and excretion were studied at three levels of renal perfusion pressure (RPP; 100, 125 and 150 mm Hg). Renal blood flow, glomerular filtration rate, diuresis and natriuresis were lower at the three RPP levels in both L-NAME-treated groups than in the control or indomethacin-treated animals. Simultaneous administration of indomethacin plus L-NAME did not further modify the hemodynamic or excretory responses observed in the L-NAME-treated animals. These results show that chronic NO inhibition impairs the renal excretory response to changes in renal perfusion pressure, and simultaneous NO and prostaglandin synthesis inhibition does not reduce those responses further. It is concluded that, on a long-term basis, a preserved NO production, but not prostaglandin production, is critical for a normal pressure diuretic and natriuretic mechanism.

Animals↗
PubMed1995

[Effects of potassium chloride and triamterene on kaliuresis, natriuresis and diuresis in congestive heart failure].

KCl and triamterene were given to 52 patients (27 males and 25 females with CHF) aged 21-82 years. Large-dose KCl (6 g daily) apparently stimulate kaliuresis, natriuresis and diuresis. As a rule, this is associated with a rise or a fall of plasma potassium concentrations. In the latter case potassium elimination runs more actively and may involve both introduced and body's potassium. As low and moderate doses of KCl (1-4 g daily) showed neither natriuretic nor diuretic effects while enhanced kaliuresis occurred in half of the patients only, did not lower potassium concentrations in plasma they are preferable. Daily treatment with triamterene is characterized by inhibition of its K-retaining action on administration day 2-3. Within first 2 days of triamterene discontinuation all the retained K eliminates from the body. Diuretics-induced metabolic alkalosis decreased intensification of natriuresis and diuresis resultant from large-dose KCl treatment.

Adult↗
PubMed1997

[Role of spinal alpha adrenoceptor in the inhibition of renal sympathetic nerve activity and natriuresis induced by blood volume expansion in rabbits].

The effect of spinal alpha adrenoceptor blockage on the inhibition of renal sympathetic nerve activity (RSNA) and natriuresis induced by blood volume expansion was investigated in anesthetized and bilateral sinoaortic denervated rabbits. In the groups of rabbits with intrathecal injection of alpha-adrenoceptor blocker phentolamine or artificial cerebrospinal fluid the inhibition of RSNA induced by blood volume expansion were (-25.4 +/- 5.4)% and (-42.5 +/- 5.2)% respectively (P < 0.05). In the groups of rabbits with intrathecal injection of alpha 1 adtenoceptor blocker prazosin or artificial cerebrospinal fluid the inhibition of RSNA induced by blood volume expansion were (-29.3 +/- 6.1)% and (-42.5 +/- 5.2)% respectively (P < 0.05). These results suggested that both spinal alpha and alpha 1 adrenceptor blockage with attenuated the inhibition of RSNA induced by blood volume expansion. The spinal alpha 1 adrenceptor blockage with intrathecal injection of prazosin also attenuated signiticantly the natriuresis and diuresis induced by blood volume expansion (P < 0.05).

Animals↗
PubMed1997

Disprocynium24 induces a dopamine-independent, eukaliuric diuresis and natriuresis in the anaesthetized rat.

In the anaesthetized rat, intravenous administration of the isocyanine 1,1'-diisopropyl-2,4'-cyanine (disprocynium24) at doses up to 600 microg/kg resulted in marked diuresis and natriuresis without affecting urinary potassium excretion. Fractional sodium excretion was increased over 10-fold indicating a high ceiling-diuretic action. The effects of disprocynium24 on renal function were accompanied by a dose-dependent reduction in heart rate (HR) and mean arterial blood pressure (MAP). Acute administration of 600 microg/kg disprocynium24 decreased MAP by 25% and, in addition, caused a fall in glomerular filtration rate (GFR). Since i) disprocynium24 has been shown to interfere with urinary dopamine excretion (UDAV) and ii) dopamine has been implicated with the regulation of renal sodium excretion, we hypothesized that the effects of disprocynium24 might be mediated by its effects on renal dopamine handling. The following findings, however, argue against this hypothesis. First, administration of disprocynium24 in single doses up to 600 microg/kg caused a diuresis and natriuresis, but did not significantly affect U(DA)V. Second, neither the systemic nor the renal response to disprocynium24 were markedly altered by pretreatment with the dopamine D1- or D2-receptor blockers SCH23390 (10 microg x kg(-1) x min[-1]) or S(-)sulpiride (15 microg x kg(-1) x min[-1]), respectively.

Animals↗
PubMed1989

Carbachol injection into the medial preoptic area induces natriuresis, kaliuresis and antidiuresis in rats.

The microinjection of carbachol into the medial preoptic area (MPO) of the rat induced natriuresis, kaliuresis and anti-diuresis in a dose-related manner. Atropine blocked all responses to carbachol. Hexamethonium impaired the dose-response effect of carbachol on kaliuresis, but had no effect on natriuresis and enhanced the antidiuretic effect of carbachol. Nicotine alone had no effects, but pre-treatment with nicotine enhanced the responses to carbachol. These data show that activity of the muscarinic receptors of the MPO increases renal electrolyte and reduces water excretion. They also suggest that nicotinic receptors have an inhibitory effect on water excretion. Nicotine could act through mechanisms unrelated to nicotinic receptors to enhance the effect of the carbachol.

Animals↗
PubMed1997

Blockade of cytochrome P-450 epoxygenase pathway attenuates the natriuresis of N(G)-monomethyl-L-arginine infusion in the spontaneously hypertensive rat.

Previous studies demonstrated that there is increased renal synthesis of cytochrome P-450-dependent arachidonic acid metabolites in the vasculature and tubules of the Okamoto spontaneously hypertensive rat (SHR). It has also been shown that the natriuretic response of the SHR to NG-monomethyl-L-arginine (L-NMMA) infusion is exaggerated compared with that of the normotensive Wistar-Kyoto rat. The purpose of this study was to determine the roles of cytochrome P-450 epoxygenase and cyclooxygenase pathways in the natriuresis that is observed with the systemic infusion of a high dose of L-NMMA to inhibit nitric oxide synthesis in the SHR and the Wistar-Kyoto rats. After a control clearance period of 20 minutes groups of adult SHR (n = 14) were given L-NMMA (15 mg/kg bolus followed by 500 microg/kg/min continuous infusion). In other groups of SHR either ketoconazole (0.5 mg/kg, n = 9) to inhibit the renal activity of cytochrome P-450 epoxygenase pathway or indomethacin (3 mg/kg, n = 7) to inhibit cyclooxygenase activity was administered intravenously 20 minutes before the control clearance period. After the control clearance period L-NMMA was infused as previously described. Infusion of L-NMMA in the control group of SHR resulted in a significant increase in fractional excretion of sodium (FE Na from 1.78% +/- 0.24% to 6.90% +/- 0.61%). In the ketoconazole-treated group of SHR, L-NMMA infusion resulted in a significant natriuresis (from 2.22% +/- 0.58% to 4.70% +/- 0.93%); however, the natriuretic response was significantly attenuated compared with that of the control group of SHR that received only L-NMMA (delta FE Na, 2.47% +/- 0.40% vs 5.24% +/- 0.55%). Indomethacin administration did not affect the natriuretic response to L-NMMA infusion in the SHR. In conclusion, the natriuretic response to L-NMMA infusion in the SHR is significantly attenuated by administration of ketoconazole but not indomethacin. This result suggests that the natriuretic effect of L-NMMA infusion in the SHR is mediated at least partly by cytochrome P-450 metabolites of the epoxygenase pathway.

Age Factors↗
PubMed1982

Aldosterone and the enhanced natriuresis of hypertonic infusions in the dog.

The purpose of this study was to determine whether small elevations in plasma sodium concentration (PNa) were effective in decreasing aldosterone secretion and, hence, in increasing sodium excretion in dogs fed normal sodium diets. Ten dogs fed a normal sodium diet, six DOCA-treated dogs, and four adrenalectomized dogs were given the same sodium load (2.5 mmol/kg) either as a hypertonic (1 M NaCl) or hypotonic (0.1 M NaCl) infusion. In all three groups of dogs, PNa was greater after the hypertonic than after the hypotonic infusion during most of the 22-h experiment. The dogs fed a normal sodium diet responded to the elevation in PNa (hypertonic infusion) with decreased aldosterone excretion and an exaggerated natriuresis. When aldosterone levels were maintained constant by either DOCA treatment or adrenalectomy, the exaggerated natriuresis that accompanied the hypertonic infusion was prevented. Therefore, elevation of PNa appears to be an important determinant of aldosterone secretion and, hence, of sodium excretion in conscious dogs fed normal sodium diets.

Adrenalectomy↗
PubMed1985

Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm.

We studied the sodium balance and changes in plasma volume by an isotope dilution technique in the first week after an aneurysmal subarachnoid hemorrhage in 21 patients. In 11 of the patients, the plasma volume decreased by more than 10%. This was accompanied by a negative sodium balance and hyponatremia in 6 patients, a negative sodium balance without hyponatremia in 4 patients, and a positive sodium balance in 1 patient. Together with a decrease in plasma volume, blood urea nitrogen content increased and body weight decreased. Three patients developed hyponatremia without a decrease in plasma volume. Serum vasopressin was measured in 14 of the 21 patients. The values were elevated on admission and declined in the first week, regardless of the presence of hyponatremia. These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction.

Arginine Vasopressin↗
PubMed1986

Importance of circulating and urinary tissue kallikrein in the control of acute natriuresis and diuresis evoked by water immersion in man.

In ten human subjects water immersion produced a two-fold diuresis and a three-fold increase in sodium secretion together with a marked fall in plasma renin activity and aldosterone. In contrast, circulating and urinary (active and total kallikrein) remained unchanged throughout the immersion period. Our results indicate that the acute diuresis and natriuresis evoked by water immersion in man is not regulated by circulating or urinary tissue kallikrein.

Adult↗
PubMed1978

No relation between atrial natriuresis and renal blood flow in conscious dogs.

Conscious dogs were used to study whether changes in total renal hemodynamics are responsible for diuresis and natriuresis during an experimental increase in left atrial pressure (LAP). To ensure a controlled dietary sodium intake, the dogs (n = 8) were chronically kept on a high or a low sodium intake diet (HSI; LSI). After the dogs had completely recovered from surgery (carotid loop, thoracotomy, flank incision), LAP was increased by about 10 cm H2O for 60 min by tightening a purse string around the mitral annulus (51 expts.). Mean urine volume (V) increased in both groups to a comparable degree. Mean sodium excretion increased somewhat more in HSI dogs, but remained elevated in LSI dogs after the LAP increase. Renal blood flow (electromagnetic flow transducer) and inulin clearance did not change. Renal vascular resistance (RVR) increased by about 20% (HSI) and 15% (LSI). --When the induced LAP INCREASE WAS TERMINATED, V decreased. RVR decreased in HSI dogs by about -11% and in LSI dogs by about -6% below control values. --It is concluded that volume regulatory mechanisms induced by an experimental LAP increase operate independently of changes in total renal blood flow.

Animals↗
PubMed1976

On the role of the decreased renal vascular resistance in the mechanism of volume natriuresis.

Acute hypophysectomy (AH) prevented the increase of the cardiac output, renal cortical blood flow (e.g. the decrease of the renal vascular resistance) and renal sodium excretion during the ECFV expansion. The non-occurrence of natriuresis in AH rats is suggested as being partly in causal relation to the inability to decrease the renal vascular resistance and thus to increase the peritubular hydrostatic pressure.

Animals↗
PubMed2000

Normal kidney function and elevated natriuresis in young men born with low birth weight.

The aim of our study was to characterize renal function and its relationship to blood pressure in healthy young Caucasian men born with a birth weight under 2,500 g (LBW). Urinary protein patterns, N-acetylglucosamine and gamma-glutamyltransferase activities, fractional sodium and potassium excretions, glomerular filtration rate, blood pressure, and erythrocyte Na+/K+-ATPase activities were determined in 65 subjects, of whom 49 were born with LBW. Signs of glomerular or tubular damage were not detected in the LBW population. However, the blood pressure and the renal sodium excretion were inversely correlated to the subjects' birth weight and were higher in LBW subjects than in controls. In contrast, the erythrocyte Na+/K+-ATPase activities were lower in LBW subjects. An inverse correlation was detected between the subjects' Na+/K+-ATPase activities and the renal sodium excretion or blood pressure. In summary, our results suggest that: (1) in young LBW Caucasian males signs of early glomerular and tubular impairment are not present; (2) the elevated renal sodium excretion may be a result of higher blood pressure; (3) the alteration of Na+/K+-ATPase activity might play a role either in the elevation of blood pressure and/or in the enhanced natriuresis of LBW subjects.

Adult↗
PubMed2002

The autonomic nervous system and pressure-natriuresis in cardiovascular-renal interactions in response to salt.

The maintenance of cardiovascular homeostasis represents a balance of activities between of the heart, vascular system and the kidneys in the control of extracellular fluid volume and ultimately blood pressure. Any disturbance in the function of these organs can lead to hypertension and heart failure. Interaction between the cardiovascular and renal systems is exerted dynamically by the autonomic nervous system and humoral factors which together determine the slope of the pressure-natriuresis relationship. This allows the body to ensure that dietary sodium intake can be excreted efficiently without causing major changes in blood pressure. Autonomic control of the kidney is exerted via the renal sympathetic nerves modulating renin release, sodium reabsorption and renal haemodynamics. Epidemiological studies have suggested a weak relationship between the level of dietary sodium intake and the development of hypertension, the underlying mechanisms are uncertain. It is evident from experimental studies that an elevation in dietary sodium intake during the growing phase heightens neural control of blood pressure and the kidney partly due to an enhanced role of the brain renin-angiotensin system. The relationship between dietary sodium and the autonomic regulation of blood pressure and the kidney is increasingly recognised as important but is only poorly understood.

Animals↗
PubMed1991

Different mechanisms of polyuria and natriuresis associated with paroxysmal supraventricular tachycardia.

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.

Adult↗