Evidence for a Renomedullary Vasodepressor Hormone

Thomas, Collen J.; Woods, Robyn L.; Evans, Roger G.; Alcorn, Daine; Christy, Irene J.; Anderson, Warwick P.

doi:10.1111/j.1440-1681.1996.tb01179.x

Cited by 29 publications

(36 citation statements)

References 56 publications

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“…8,11 Cytochrome P450 inhibitors also abolish the depressor response in rats to intravenous administration of renal venous effluent from high pressure-perfused rat isolated kidneys, either when the perfused kidney is treated with ketoconazole, 12 or when the assay rat is treated with SKF 525A. 13 Taken together, these and other data 3,4,6 have been interpreted to indicate that a lipid pro-hormone (medullipin I) is synthesised within the kidney (presumably the medulla) and converted to the active depressor substance (medullipin II) within the liver. Both the synthesis of medullipin I in the kidney and its conversion to medullipin II in the liver appear to be dependent on the actions of cytochrome P450.…”

supporting

confidence: 59%

“…3,4 There is extensive evidence that these renal antihypertensive mechanisms act in concert with other cardiovascular homeostatic factors in the control of arterial pressure. 2,4 -6 The hormonal antihypertensive response to increased RPP has been a matter of intense study for the past 45 years, yet the nature of this substance remains to be characterized biochemically.…”

mentioning

confidence: 99%

“…2,4 -6 The hormonal antihypertensive response to increased RPP has been a matter of intense study for the past 45 years, yet the nature of this substance remains to be characterized biochemically. 4,6 Recently, evidence has accumulated for the involvement of cytochrome P450 enzyme systems in its expression. The rapid normalization of blood pressure after unclipping the renal artery of a 1-kidney, 1-clip hypertensive rat is potentiated by induction of cytochrome P450 systems by phenobarbital, 7 and by the dual inhibitor of cyclooxygenase and lipoxygenase BW755C.…”

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confidence: 99%

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Effects of Intrarenal Infusion of 17-Octadecynoic Acid on Renal Antihypertensive Mechanisms in Anesthetized Rabbits

Evans

Day

Roman

et al. 1998

American Journal of Hypertension

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To characterize the role of cytochrome P450 metabolism of fatty acids in the renal response to increased renal perfusion pressure, we tested the effects of renal arterial infusion of 17-octadecynoic acid (17-ODYA, 450 nmol/min) on renal and systemic hemodynamic, and renal excretory responses to step-wise increases in renal perfusion pressure (RPP) in anesthetized rabbits, using an extracorporeal circuit for renal autoperfusion. Inhibition of cytochrome P450-dependent fatty acid metabolism was estimated by comparing the metabolism of arachidonic acid in microsomes prepared from the kidneys of control and 17-ODYA-treated animals.Step-wise increases in RPP decreased mean arterial pressure, which previous studies have indicated is attributable to the release of a depressor hormone from the renal medulla. Elevations in RPP also increased renal blood flow and glomerular filtration rate, and the absolute and fractional excretions of urine and sodium. Intrarenal infusion of 17-ODYA reduced the metabolism of arachidonic acid to 20-hydroxyeicosatetraenoic acid by 41%, but it did not significantly influence the responses to increased renal perfusion pressure. We conclude that either the responses elicited by increased renal perfusion pressure in anesthetized rabbits do not depend on cytochrome P450-dependent fatty acid metabolism, or that cytochrome P450 activity must be inhibited by more than was achieved in the present study (41%), before functional effects on the response to increased renal perfusion pressure are observed. Am J Hypertens 1998;11:803-812

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confidence: 59%

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confidence: 99%

mentioning

confidence: 99%

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Effects of Intrarenal Infusion of 17-Octadecynoic Acid on Renal Antihypertensive Mechanisms in Anesthetized Rabbits

Evans

Day

Roman

et al. 1998

American Journal of Hypertension

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“…Nevertheless, we cannot as yet completely exclude the possibility that some other action of NE in the renal medulla, such as a direct action on renal medullary interstitial cells, the proposed site of storage and release of medullipin, 12 inhibits the release of the putative renal medullary depressor hormone. However, given our previous finding that medullary interstitial infusion of [Phe, 2 Ile, 3 Orn 8 ]vasopressin reduces MBF and attenuates the depressor response to increased RAP, 2 a role for the medullary microvasculature seems worthy of further investigation.…”

Section: Putative Renal Medullary Depressor Hormonementioning

confidence: 97%

“…This response has been extensively characterized previously and appears to be unrelated to the accompanying inhibition of the renin-angiotensin system 3 or increase in U VOL and U Na ϩ V. 2,4 On the basis of the finding that the depressor response is abolished by chemical medullectomy, 4 we have proposed that this response to increased RAP is mediated chiefly by release of an as-yet-to-be-characterized depressor hormone from the renal medulla. 12 It may be that this putative hormone is identical, or similar, to "medullipin," which has been isolated but not yet fully chemically characterized. 13 Previous studies have shown that some, 2,14,15 but not all, stimuli that reduce MBF 11,16 attenuate the depressor response to increased RAP.…”

Section: Putative Renal Medullary Depressor Hormonementioning

confidence: 99%

Effects of Renal Medullary and Intravenous Norepinephrine on Renal Antihypertensive Function

et al. 2000

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Abstract-Increasing renal arterial pressure activates at least 3 antihypertensive mechanisms: reduced renin release, pressure natriuresis, and release of a putative renal medullary depressor hormone. To examine the role of renal medullary perfusion in these mechanisms, we tested the effects of the infusion of norepinephrine, either infusion into the renal medullary interstitium or intravenous infusion, on responses to increased renal arterial pressure in pentobarbital-anesthetized rabbits. We used an extracorporeal circuit, which allows renal arterial pressure to be set to any level above or below systemic arterial pressure. With renal arterial pressure initially set at 65 mm Hg, intravenous and medullary interstitial norepinephrine (300 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 ) similarly increased mean arterial pressure (by 12% to 17% of baseline) and reduced total renal blood flow (by 16% to 17%) and cortical perfusion (by 13% to 19%), but only medullary norepinephrine reduced medullary perfusion (by 28%). When renal arterial pressure was increased to Ϸ160 mm Hg, in steps of Ϸ65 mm Hg, urine output and sodium excretion increased exponentially, and plasma renin activity and mean arterial pressure fell. Medullary interstitial but not intravenous norepinephrine attenuated the increased diuresis and natriuresis and the depressor response to increased renal arterial pressure. This suggests that norepinephrine can act within the renal medulla to inhibit these renal antihypertensive mechanisms, perhaps by reducing medullary perfusion. These observations support the concept that medullary perfusion plays a critical role in the long-term control of arterial pressure by its influence on pressure diuresis/natriuresis mechanisms and also by affecting the release of the putative renal medullary depressor hormone. Key Words: kidney medulla Ⅲ laser-Doppler flowmetry Ⅲ norepinephrine Ⅲ natriuresis Ⅲ renal circulation I t has been hypothesized that the level of medullary blood flow (MBF) is an important determinant of urinary sodium excretion (U Na ϩ V) and, indeed, may be the key initiating factor in the pressure natriuresis response. 1 In turn, the impact of MBF on the pressure natriuretic mechanism provides an explanation for the effects of chronic changes in MBF on the long-term control of arterial pressure. 1 Thus, in rats, chronic reductions in MBF shift the pressure natriuresis relation toward higher pressures and lead to hypertension in normotensive animals. Conversely, chronic increases in MBF shift the pressure natriuresis relation toward lower pressures and ameliorate hypertension in spontaneously hypertensive rats. 1 From studies using an extracorporeal circuit in anesthetized rabbits, 2 we recently obtained preliminary evidence indicating that influences on the release and/or actions of the putative renal medullary depressor hormone might also contribute to the impact of MBF on the long-term control of arterial pressure. In this model, 3 major renal antihypertensive mechanisms can be studied simultaneously. Thus, when renal arterial ...

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Renal Medullary Circulation

Pallone

Edwards

Mattson

2012

Comprehensive Physiology

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The renal medullary microcirculation is a distinctive arrangement of blood vessels that serve multiple functions in the renal medulla. This article begins with a description of the unique anatomy of this vascular bed and the role it plays in transport and countercurrent exchange in the medulla. A segment of the review is then devoted to the important role mathematical modeling has played in the understanding of this vascular bed's function. Succeeding sections focus upon the hematocrit in the vasa recta capillaries and methods utilized to assess blood flow in the renal medulla. An extensive portion of the article is then devoted to the regulation of the medullary circulation, from ion channel architecture to neurohormonal signaling. Finally, we discuss the importance of the renal medullary circulation in the regulation of fluid and electrolyte homeostasis and arterial blood pressure regulation.

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Evidence for a Renomedullary Vasodepressor Hormone

Cited by 29 publications

References 56 publications

Effects of Intrarenal Infusion of 17-Octadecynoic Acid on Renal Antihypertensive Mechanisms in Anesthetized Rabbits

Effects of Intrarenal Infusion of 17-Octadecynoic Acid on Renal Antihypertensive Mechanisms in Anesthetized Rabbits

Effects of Renal Medullary and Intravenous Norepinephrine on Renal Antihypertensive Function

Renal Medullary Circulation

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