Natriuresis caused by increased carotid Na+ concentration after renal denervation

Emmeluth, Claus; Goetz, K. L.; Drummer, C.; Gerzer, R.; Forssmann, W. G.; Bie, Ping

doi:10.1152/ajprenal.1996.270.3.f510

Cited by 13 publications

(14 citation statements)

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“…We therefore suggest that a substantial part of the natriuresis induced by hypertonic saline loading must be attributed to the increased osmotic concentration rather than to the change in body fluid volume. Previous investigations from our laboratory also support the concept of such a concentration-mediated natriuresis in dogs (20)(21)(22)(23) as well as in humans (4,6,10). However, in our recent human investigations using a design very similar to the present, hypertonic and isotonic saline induced natriuretic responses that were statistically indistinguishable.…”

Section: Discussionsupporting

confidence: 78%

“…13,27,39). The efferent signal in the natriuresis of central osmostimulation is most likely mediated by a humoral factor because renal denervation does not abolish the natriuresis of osmostimulation (22), but this factor has not been positively identified. In the present study, we measured several well-known mediators of sodium excretion to clarify the mechanism of the osmostimulated natriuresis.…”

Section: Discussionmentioning

confidence: 99%

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Natriuresis induced by mild hypernatremia in humans

Andersen

Pump

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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The hypothesis that increases in plasma sodium induce natriuresis independently of changes in body fluid volume was tested in six slightly dehydrated seated subjects on controlled sodium intake (150 mmol/day). NaCl (3.85 mmol/kg) was infused intravenously over 90 min as isotonic (Iso) or as hypertonic saline (Hyper, 855 mmol/l). After Hyper, plasma sodium increased by 3% (142.0 +/- 0.6 to 146.2 +/- 0.5 mmol/l). During Iso a small decrease occurred (142.3 +/- 0.6 to 140.3 +/- 0.7 mmol/l). Iso increased estimates of plasma volume significantly more than Hyper. However, renal sodium excretion increased significantly more with Hyper (291 +/- 25 vs. 199 +/- 24 micromol/min). This excess was not mediated by arterial pressure, which actually decreased slightly. Creatinine clearance did not change measurably. Plasma renin activity, ANG II, and aldosterone decreased very similarly in Iso and Hyper. Plasma atrial natriuretic peptide remained unchanged, whereas plasma vasopressin increased with Hyper (1.4 +/- 0.4 to 3.1 +/- 0.5 pg/ml) and decreased (1.3 +/- 0.4 to 0.6 +/- 0.1 pg/ml) after Iso. In conclusion, the natriuretic response to Hyper was 50% larger than to Iso, indicating that renal sodium excretion may be determined partly by plasma sodium concentration. The mechanism is uncertain but appears independent of changes in blood pressure, glomerular filtration rate, the renin system, and atrial natriuretic peptide.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Natriuresis induced by mild hypernatremia in humans

Andersen

Pump

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Blood (18 ml) was sampled at 10-min intervals for determination of plasma concentrations of norepinephrine (NE), epinephrine (E), arginine vasopressin (AVP), and plasma osmolality as previously described (5,12,20). The catheter was thereafter flushed with 18 ml of isotonic saline.…”

Section: Methodsmentioning

confidence: 99%

Central volume expansion is pivotal for sustained decrease in heart rate during seated to supine posture change

Pump

Kamo

Gabrielsen

et al. 2001

American Journal of Physiology-Heart and Circulatory Physiology

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During prolonged, static carotid baroreceptor stimulation by neck suction (NS) in seated humans, heart rate (HR) decreases acutely and thereafter gradually increases. This increase has been explained by carotid baroreceptor adaptation and/or buffering by aortic reflexes. During a posture change from seated to supine (Sup) with similar carotid stimulation, however, the decrease in HR is sustained. To investigate whether this discrepancy is caused by changes in central blood volume, we compared (n = 10 subjects) the effects of 10 min of seated NS (adjusted to simulate carotid stimulation of a posture change), a posture change from seated to Sup, and the same posture change with left atrial (LA) diameter maintained unchanged by lower body negative pressure (Sup + LBNP). During Sup, the prompt decreases in HR and mean arterial pressure (MAP) were sustained. HR decreased similarly within 30 s of NS (65 +/- 2 to 59 +/- 2 beats/min) and Sup + LBNP (65 +/- 2 to 58 +/- 2 beats/min) and thereafter gradually increased to values of seated. MAP decreased similarly within 5 min during Sup + LBNP and NS (by 7 +/- 1 to 9 +/- 1 mmHg) and thereafter tended to increase toward values of seated subjects. Arterial pulse pressure was increased the most by Sup, less so by Sup + LBNP, and was unchanged by NS. LA diameter was only increased by Sup. In conclusion, static carotid baroreceptor stimulation per se causes the acute (<30 s) decrease in HR during a posture change from seated to Sup, whereas the central volume expansion (increased LA diameter and/or arterial pulse pressure) is pivotal to sustain this decrease. Thus the effects of central volume expansion override adaptation of the carotid baroreceptors and/or buffering of aortic reflexes.

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“…The intra-assay coefficient of variation (c.v.) in the urine and plasma assay runs were 14 and 10%, respectively, at an ET-1 concentration of 6 pg ml-' in urine and plasma. Immunoreactivity of AVP in plasma was determined by the technique described by Emmeluth et al (1996) using an antibody (WAR) described earlier (Andersen, Andersen, Schiitten, Warberg & Bie, 1990). The detection limit was <0'15 pg per tube.…”

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confidence: 99%

Natriuretic effect of non‐pressor doses of endothelin‐1 in conscious dogs.

Sandgaard

Bie

1996

The Journal of Physiology

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1. Renal, endocrine and haemodynamic responses to separate intravenous infusions of three doses of endothelin-1 (40, 400 and 4000 fmol kg-' min-') were investigated in conscious dogs.2. Administration of 40, 400 and 4000 fmol kg-1 min-' endothelin-1 for 120 min increased plasma endothelin-1 levels by two-, seven-and 250-fold, respectively. 3. The two low doses did not have measurable effects on mean arterial blood pressure and heart rate but tended to increase glomerular filtration rate. The high dose increased mean arterial blood pressure (MABP; from 104 + 4 to 138 + 4 mmHg, P < 0 05) and decreased heart rate (from 71 + 4 to 46 + 3 beats min-l, P < 0 05) as well as glomerular filtration rate (from 47 + 3 to 19 + 5 ml min-', P< 0 05).4. At rates of 40 and 400 fmol kg-' min-', endothelin-1 increased sodium excretion about fiveand eightfold, respectively. Relative changes in fractional sodium excretion were very similar. The high dose was markedly antinatriuretic (reducing sodium excretion from 8'3 + 1P1 to 1X2 + 0-2 ,umol min-', P < 0 05).5. Diuresis increased during the administration of the two lower doses, which did not change plasma atrial natriuretic peptide or vasopressin concentrations. Urine flow increased after termination of the infusion of the pressor dose despite elevated plasma vasopressin and subnormal glomerular filtration rate.6. Infusion of endothelin-1 at 40 fmol kg-' min-' did not change the concentrations of angiotensin II and atrial natriuretic peptide in plasma. Infusion of 400 fmol kg-1 min-' was associated with a decrease in plasma angiotensin II, while plasma atrial natriuretic peptide was unchanged. The high dose of endothelin-1 markedly increased plasma levels of both hormones. 7. It is concluded that endothelin-1 at low plasma concentrations increases sodium excretion while a higher pressor dose of endothelin-1 is antinatriuretic. However, increases in plasma endothelin-1 seem to elicit diuresis over a wide concentration range, although possibly by different mechanisms.

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Natriuresis caused by increased carotid Na+ concentration after renal denervation

Cited by 13 publications

References 0 publications

Natriuresis induced by mild hypernatremia in humans

Natriuresis induced by mild hypernatremia in humans

Central volume expansion is pivotal for sustained decrease in heart rate during seated to supine posture change

Natriuretic effect of non‐pressor doses of endothelin‐1 in conscious dogs.

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