Mechanism of Effect of Alpha Adrenergic Stimulation with Norepinephrine on Renal Water Excretion

Schrier, Robert W.; Berl, Tomás

doi:10.1172/jci107207

Cited by 89 publications

(51 citation statements)

References 22 publications

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“…They interpreted their results to indicate that the antidiuresis of beta adrenergic stimulation was mediated by increased ADH secretion in response to an alteration in systemic hemodynamics. Similarly, norepinephrine did not cause a diuresis in hypophysectomized dogs receiving 80 ,uU/kg per min of vasopressin which seemed to indicate that the effect of norepinephrine on free water clearance was mediated through altering ADH secretion (35). However, norepinephrine (36), angiotensin, and renal nerve stimulation (36) are all known to increase PGE synthesis and, as we have found, an infusion of 80 ,uU/kg per min of vasopressin may block the demonstration of ADH antagonism.…”

Section: Resultssupporting

confidence: 58%

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Galvez¹,

Roberts²,

Mishkind³

et al. 1977

J. Clin. Invest.

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A B S T R A C T Acute renal artery stenosis in hydropenic dogs caused a contralateral increase in urine volume and free water clearance without change in glomerular filtration, renal blood flow, or osmolar clearance. The increase in urine volume was not dependent on the development of hypertension since it occurred in animals pretreated with trimethaphan but was dependent upon angiotensin since it was prevented with angiotensin blockade with Saralasin. The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 uU/kg per min of aqueous Pitressin. Since the rise in urine volume was associated with an increase in renal vein prostaglandin E concentration and was prevented by pretreatment with indomethacin (5 mg/kg) the results suggest that the rise in plasma angiotensin after renal artery stenosis causes an increase in contralateral prostaglandin E synthesis with resultant antagonism to antidiuretic hormone at the collecting tubule.

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Section: Resultssupporting

confidence: 58%

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Galvez¹,

Roberts²,

Mishkind³

et al. 1977

J. Clin. Invest.

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“…15 Increased sympathetic drive contributes to avid sodium and water retention through renal vasoconstriction, stimulation of the renin-angiotensin-aldosterone system, and a direct effect on the proximal convoluted tubule. 15,16 Increased angiotensin II and aldosterone levels in heart failure lead to decreased sodium and water delivery to the collecting duct, which, combined with resistance to the action of natriuretic peptides, result in impairment of free-water excretion and hyponatremia. 15 Finally, the nonosmotic stimulation of vasopressin release leads to elevated vasopressin concentration, which results in an increased number of aquaporin water channels in the collecting duct of the kidney that promote abnormal free water retention and contribute to the development of hyponatremia.…”

Section: Discussionmentioning

confidence: 99%

Lower Serum Sodium Is Associated With Increased Short-Term Mortality in Hospitalized Patients With Worsening Heart Failure

et al. 2005

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MD; for the OPTIME-CHF InvestigatorsBackground-The prognostic value of serum sodium in patients hospitalized for worsening heart failure has not been well defined. Methods and Results-The Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic HeartFailure (OPTIME-CHF) study randomized 949 patients with systolic dysfunction hospitalized for worsening heart failure to receive 48 to 72 hours of intravenous milrinone or placebo in addition to standard therapy. In a retrospective analysis, we investigated the relationship between admission serum sodium and the primary end point of days hospitalized for cardiovascular causes within 60 days of randomization, as well as the secondary end points of in-hospital mortality, 60-day mortality, and 60-day mortality/rehospitalization. The number of days hospitalized for cardiovascular causes was higher in the lowest sodium quartile: 8.0 (4.5, 18.5) versus 6 (4, 13) versus 6 (4, 11.5) versus 6 (4, 12) days (PϽ0.015 for comparison with the lowest quartile). Lower serum sodium was associated with higher in-hospital and 60-day mortality: 5.9% versus 1% versus 2.3% versus 2.3% (PϽ0.015) and 15.9% versus 6.4% versus 7.8% versus 7% (Pϭ0.002), respectively. There was a trend toward higher mortality/rehospitalization for patients who were in the lowest sodium quartile. Multivariable-adjusted Cox proportional hazards analysis showed that serum sodium on admission, when modeled linearly, predicted increased 60-day mortality: sodium (per 3-mEq/L decrease) had a hazard ratio of 1.18 with a 95% CI of 1.03 to 1.36 (Pϭ0.018). Conclusions-In patients hospitalized for worsening heart failure, admission serum sodium is an independent predictor of increased number of days hospitalized for cardiovascular causes and increased mortality within 60 days of discharge.

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“…It has been known that noradrenaline has a direct inhibitory effect on supraoptic neurosecretory cells of the cat (BARKER et al, 1971) and that noradrenaline induces water diuresis ascribable to a suppression of vasopressin in the dog (SCHRIER and BERL, 1973). However, the latter authors further ascribed this effect of noradrenaline to altering autonomic baroreceptor tone (BERL et a!.,1974).…”

Section: Discussionmentioning

confidence: 99%

Conditions for secretion of vasopressin in pressor amounts in water-replete rats.

Iriuchijima

1983

Jpn.J.Physiol

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Conditions for secretion of pressor amounts of vasopressin were sought in conscious, water-replete rats. The characteristic lowering of arterial pressure on injection of a vasopressin antagonist was used to detect vasopressin secretion in pressor amounts. The absence or marked abatement of both baroreceptor impulses and adrenomedullary secretion were found necessary for secretion of vasopressin in pressor amounts : the vasopressin antagonist lowered arterial pressure in rats with sinoaortic denervation and ganglion blockade or adrenalectomy. Besides baroreceptor activity and adrenomedullary secretion, anesthetics were also found inhibitory on vasopressin release in pressor amounts. The adrenomedullary hormone signaling the presence of adrenomedullary activity to the vasopressin releasing mechanism was identified as noradrenaline and not adrenaline. It is suggested that the vasopressin pressor mechanism is recruited to sustain arterial pressure when the sympathoadrenal system fails.

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Mechanism of Effect of Alpha Adrenergic Stimulation with Norepinephrine on Renal Water Excretion

Cited by 89 publications

References 22 publications

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Studies of the mechanism of contralateral polyuria after renal artery stenosis.

Lower Serum Sodium Is Associated With Increased Short-Term Mortality in Hospitalized Patients With Worsening Heart Failure

Conditions for secretion of vasopressin in pressor amounts in water-replete rats.

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