Natriuretic “hormone” and the renal prostaglandins

Lee, James B.

doi:10.1016/0090-6980(72)90065-2

Cited by 54 publications

(9 citation statements)

References 35 publications

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“…For a more detailed discussion of this subject the reader is referred to several recent reviews [38][39][40]. A hypothetical schema which is at least partially supported by experimental observations is shown in figure 6 whereby circulating PGA may normally exert an antihypertensive endocrine effect.…”

Section: Resultsmentioning

confidence: 88%

“…Interestingly, indomethacin has been shown to result in a pattern of renal hemodynamic change which is the reverse of that of PG A: a reduction in inner cortical blood flow and a rise in blood pressure. Such mediation of natriuresis by PGA2 (and/or PGE2) has led to speculation that these compounds may represent the so-called elusive natriuretic hormone [38].…”

Section: Renalmentioning

confidence: 99%

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Renal Prostaglandins

Lee¹,

Attallah²

1975

Nephron

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The renal prostaglandins PGA₂ and PGE₂ possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA₁ and PGA₂. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as ‘ideal’ antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.

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Section: Resultsmentioning

confidence: 88%

Section: Renalmentioning

confidence: 99%

Renal Prostaglandins

Lee¹,

Attallah²

1975

Nephron

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“…Following the discovery and characterization of the prostaglandins, numerous proposals have been advanced suggesting that prostaglandins may par- ticipate in modulating renal sodium handling (Gross and Bartter, 1973;Lee, 1972;Vander, 1968). Thus, Lee (1972) proposed that the natriuresis which followed ECVE is mediated, at least in part, by en- …”

Section: Discussionmentioning

confidence: 99%

“…Thus, Lee (1972) proposed that the natriuresis which followed ECVE is mediated, at least in part, by en- …”

Section: Discussionmentioning

confidence: 99%

Relationship between renal prostaglandin E and renal sodium handling during water immersion in normal man.

Epstein¹,

Lifschitz²,

Hoffman³

et al. 1979

Circulation Research

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SUMMARY Previous studies from this laboratory have demonstrated that the central hypervolemia induced by water immersion to the neck (NI) constitutes a suitable model for assessing the hormonal response to volume expansion without concomitant alterations in plasma composition. The NI model was used to assess in a kinetic fashion the relationship between renal prostaglandin E (PGE) and renal sodium handling. Nine normal subjects were studied twice in the sodium-replete state during NI: with indomethacin (Ind) pretreatment (50 mg q6h x 6)(NI + Ind) and without indomethacin (NI). Urinary sodium, potassium, and PGE excretion (UPGEV) were measured hourly. NI was associated with marked increases in U N .V [from 87 ± 20 (SE) to 219 ± 25 pEq/min (P < 0.06)] and UpG K V[from 6.4 ± 1.4 to 12.9 ± 2.5 ng/min (P < 0.05)]. Although indomethacin administration lowered the basal rate of UPGBV prior to immersion, it neither prevented the subsequent augmentation of UPGEV during NI + Ind nor affected the magnitude of the natriuresis during NI + Ind. Subsequently, six of the subjects were restudied following dietary sodium restriction (10 mEq/day). The changes in UPGBV during NI and NI + Ind were qualitatively similar to those observed in the sodium-replete state. In contrast to the sodium-replete studies, however, the natriuresis of immersion was attenuated markedly by indomethacin pretreatment. In summary, the data demonstrate that immersion-induced central volume expansion is associated with a striking increase in renal PGE excretion which is attenuated but not prevented by indomethacin. In addition, indomethacin administration attenuates markedly the natriuretic response of immersion in sodium-depleted, but not in sodium-replete, normal subjects. These observations are consistent with the suggestion that renal PGE may constitute a determinant of the renal response to volume expansion in sodium-depleted man. Circ Res 45: 71-80, 1979 DESPITE extensive study, the relationship of the renal synthesis of prostaglandins to renal sodium excretion remains controversial (Dunn and Hood, 1977). Although it has been proposed that alterations in prostaglandin release may constitute a determinant of the natriuretic response to extracellular fluid volume expansion (ECVE) (Gross and Bartter, 1973; Verberckmoes et al., 1976; Donker et al., 1976;Patak et al., 1975; Berg, 1977; Diising et al., 1976), the effect of volume expansion on endogenous prostaglandin release and the contribution of endogenous renal prostaglandins to the natriuresis of volume expansion remain unsettled (Kirschenbaum and Stein, 1977;Mountokalakis et al., 1978; Bohan and Wesson, 1976). The contradictory nature of the available data may relate in part to species differences and to attempts to extrapolate from studies in anesthetized or acutely operated animals to man. The present studies were carried out to examine in a kinetic fashion the effect(s) of a "volume stimulus" on renal prostaglandin synthesis and the relationship of renal prostaglandins to the resultant natriur...

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“…Recently, Lee (1971Lee ( , 1972 proposed a hypothesis that PGA may be a circulatory natriuretic antihypertensive hormone of renal origin. On the other hand, it has also been suggested that PGE2 may be a modulator of the excretory function of the kidney (Fulgraff et al 1974).…”

mentioning

confidence: 99%