Influence of renal prostaglandin synthesis on renin control mechanisms in the dog.

Seymour, A A; Zehr, J. E.

doi:10.1161/01.res.45.1.13

Cited by 53 publications

(28 citation statements)

References 40 publications

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“…With partial aortic constriction, however, the effects of these inhibitors on renal hemodynamics and APR were readily apparent, not surprisingly since this maneuver leads to prompt stimulation and renal release of endogenous PG and All (21)(22)(23)(24)(25)(26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

“…As with fluid movement across extrarenal capillary beds, rates of filtration and absorption of fluid across renal glomerular and peritubular capillaries are governed by local imbalances in transcapillary hydraulic and colloid osmotic pressures (the so-called Starling forces) (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17) (21)(22)(23)(24)(25)(26)(27)(28); both hormone systems are capable of altering glomerular and postglomerular Starling forces substantially (18)(19)(20)(29)(30)(31)(32)(33)(34). The present study was therefore designed to evaluate the roles played by these endoge-I)ous renal vasoactive substances in mediating the close coupling betweeni CFR and APR that occurs in response to partial aortic constriction in the Munich-Wistar rat.…”

Section: Introductionmentioning

confidence: 99%

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Importance of Efferent Arteriolar Vascular Tone in Regulation of Proximal Tubule Fluid Reabsorption and Glomerulotubular Balance in the Rat

Ichikawa¹,

Brenner²

1980

J. Clin. Invest.

102

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A B S T R A C T Micropunctre study was performed in 21 mildly volumne-expanded Mlunich-Wistar rats before and during partial aortic constriction to examine the effects of endogenious prostaglandins (PG) and angiotenisin II (All) on single nephron glomerular filtration rate (SNGFR) and al)solute proximal reabsorption rate (APR). Animilals received either vehicle (group 1), indomethacini (group 2), or indomethacin plus saralasin (group 3). Before aortic constriction, these inhibitors were without effect on values of SNGFR and APR. In grouip 1 rats, reduction in mean renal arterial perfusion pressture (RAP) to -65 mm Hg resulted in m-arked and prop)ortional declines in SNGFR and APR. With equivalent re(duiction in RAP in grouip 2 rats, however, SNGFR fell to a lesser extent and APR tended to increase slightly above preconstriction values. Indomethacin admiiinistration was therefore associated with disruption of' glomerulotubular balance. In view of the roughly e(lllivalent dleclines in afferent arteriolar resistance measture(d in grouips 1 aind( 2, the milagnittude of increase in efferen1t arteriolar resistaince (RE) appeared to be of imiajor importance in determiiining the observed presence or ahsence of glomeruilottubuilar balance. Thus, the lesser filtl in SNGFR in grouip 2 thain in grouip 1 was a resuilt of' the higher value for glomeruilar capillarv hydrauilic pressture in grouip 2, a conseqtuence of the higlher value of RE. The higher average value Portions of' these stuidies were presented at the Eastern Section

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Importance of Efferent Arteriolar Vascular Tone in Regulation of Proximal Tubule Fluid Reabsorption and Glomerulotubular Balance in the Rat

Ichikawa¹,

Brenner²

1980

J. Clin. Invest.

102

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“…Species differences may also be responsible for some of these inconsistencies, as in the dog denervated kidney intrarenal infusion of indomethacin markedly reduced prostaglandin secretion and renin activity in the venous effluent and attenuated the renin response to intravenous frusemide (Seymour & Zehr, 1979). Also in the intact animal a fall in plasma potassium concentration following frusemide administration could stimulate renin release and there is some evidence that this response is mediated by prostaglandins (Lazar & Whorton, 1980).…”

Section: Discussionmentioning

confidence: 99%

Frusemide releases renin in the rat kidney when prostacyclin synthesis is suppressed

Barden

Mahoney

Tunney

et al. 1984

British J Pharmacology

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1 The effect of inhibiting prostaglandin (PG) synthesis on basal and frusemide-stimulated renin secretion was examined in the rat isolated perfused kidney. The stable PGI2 derivative, 6-keto PGF1,, was measured by radioimmunoassay in urine collected from the kidney.2 Treatment of rats with indomethacin (3.0mgkg-1) reduced 6-keto PGF1< excretion from 121.3±39.1(n=9) to 15.5±6.6(n=9)pgmin-1(P<0.02) but had no effect on basal renin secretion. Renal perfusion pressure, flow rate and vascular resistance were similar in treated and control rats. Mean urine flow was lower after treatment.3 Infusion of frusemide (250 gmin-1) did not alter 6-keto PGFi,, excretion in control or indomethacin-treated (P> 0.05) rats. Although renin secretion was increased during frusemide infusion, there was no significant difference between control (1,806 ± 384 ng angiotensin I (Al) min-') and treated (2,310±554ng AImin-) rats (P>0.05). Propranolol, at a dose (81Lgmin-1) which suppressed renin secretion after isoprenaline stimulation, had no effect on the response to frusemide in indomethacin-treated rats. 4 These results demonstrate that frusemide-stimulated renin secretion in the rat kidney does not require intact renal PGI2 synthesis and is independent of f3-adrenergic mechanisms.

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“…8 ' 8> 101 lI It seems likely that the renal prostaglandins function as primary stimuli for renin release, both by a direct action on the juxtaglomerular (JG) cells 2 "* and possibly also by an indirect action to amplify or attenuate the signal for other receptor mechanisms, i.e., prostaglandins alter both urinary electrolyte excretion and renal arteriolar tone 4 ia and thus might indirectly influence the macula densa and the renal vascular receptor, respectively.…”

mentioning

confidence: 99%

“…In adrenalectomized dogs with a single denervated nonfiltering kidney, a preparation in which the renal vascular receptor is isolated from the sympathetic nervous system and the macula densa," renal vein renin was increased both by reducing renal perfusion pressure and by intrarenal infusions of sodium arachidonate. 8 Pretreatment with indomethacin was reported to block the renin responses to both stimuli, and it was suggested that renal vascular receptor stimulation of renin release is mediated by a cyclooxygenase product, presumably a prostaglandin.' These acute experiments* were performed in anesthetized dogs following surgery, conditions that stimulate basal levels of renin and prostaglandin release.…”

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confidence: 99%

Renal prostaglandins and the control of renin release.

Freeman¹,

Davis²,

Dietz³

et al. 1982

Hypertension

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multifactorial. Stimuli for renin release act through three groups of mechanisms which include: 1) two intrarenal receptors, the renal vascular receptor in the afferent arteriole and the macula densa; 2) the renal nerves and a renal 0-adrenergic receptor; and 3) a group of humoral agents.1 In the past decade, attention has been focused on the potential role of the renal prostaglandins in renin release, both as primary stimuli*" 1 and as essential mediators in stimulus-secretion coupling for the renal vascular receptor, M the macula densa, 7 '• and the renal /3-adrenergic receptor. 8 ' 8> 101 lI It seems likely that the renal prostaglandins function as primary stimuli for renin release, both by a direct action on the juxtaglomerular (JG) cells 2 "* and possibly also by an indirect action to amplify or attenuate the signal for other receptor mechanisms, i.e., prostaglandins alter both urinary electrolyte excretion and renal arteriolar tone 4 -ia and thus might indirectly influence the macula densa and the renal vascular receptor, respectively. More controversial is the concept of the renal prostaglandins as essential mediators in stimulussecretion coupling for one or more of the basic receptor mechanisms in the control of renin release.11 The fundamental importance of the autonomous renal vascular receptor mechanism for renin release led to early studies of its relationship to the renal prostaglandins, and one of the first suggestions that prostaglandins function as mediators for stimulus-secretion coupling was for the renal vascular receptor." In adrenalectomized dogs with a single denervated nonfiltering kidney, a preparation in which the renal vascular receptor is isolated from the sympathetic nervous system and the macula densa," renal vein renin was increased both by reducing renal perfusion pressure and by intrarenal infusions of sodium arachidonate.8 Pretreatment with indomethacin was reported to block the renin responses to both stimuli, and it was suggested that renal vascular receptor stimulation of renin release is mediated by a cyclooxygenase product, presumably a prostaglandin.' These acute experiments* were performed in anesthetized dogs following surgery, conditions that stimulate basal levels of renin and prostaglandin release.

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Influence of renal prostaglandin synthesis on renin control mechanisms in the dog.

Cited by 53 publications

References 40 publications

Importance of Efferent Arteriolar Vascular Tone in Regulation of Proximal Tubule Fluid Reabsorption and Glomerulotubular Balance in the Rat

Importance of Efferent Arteriolar Vascular Tone in Regulation of Proximal Tubule Fluid Reabsorption and Glomerulotubular Balance in the Rat

Frusemide releases renin in the rat kidney when prostacyclin synthesis is suppressed

Renal prostaglandins and the control of renin release.

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