Vasoconstrictor-induced changes in renal blood flow: role of prostaglandins and histamine

Banks, Robert O.

doi:10.1152/ajprenal.1988.254.4.f470

Cited by 8 publications

(13 citation statements)

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“…ERBF and ERPF during MRAP increased by the vasopressor infu sion of PEP and with paired hematocrit in creases of 10.1 ± 1.6% represent evidently renal circulatory autoregulation as a com bined function of both MRAP and hemato crit change occurring simultaneously. This finding of renal hemodynamic constancy, was apparently in association with the renal blood flow escape phenomenon from a renal a-adrenergic vasoconstrictor effect, an es cape recently described by Banks [60] with norepinephrine.…”

Section: Discussionsupporting

confidence: 58%

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Waugh

1991

J Vasc Res

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The effects of renal arterial pressure change on renal output of sodium and volume were measured during water diuresis in 25 chloralose-anesthetized dogs. Conditions included a minimal invasive stress, limited sodium administration, and mean renal arterial pressures varied suprarenally, by aortic balloon inflation to lowermost levels of 82–106 mm Hg. Group A dogs received no aldosterone; group B, C and D dogs were given aldosterone. Dogs of group C also received (1-Sar, 8-Ile)-angiotensin II. Group D dogs received phenylephrine which elevated arterial and right atrial pressures moderately without decrease in renal blood flow. In groups A, B and C, mean changes in sodium output, volume output, fractional excretions and free water clearances were not detectable with mean renal arterial pressure reductions, which averaged 29 ± 2.9, 22 ± 2.8 and 27 ± 5.2 mm Hg, respectively. Right atrial pressures, effective renal blood flows and glomerular filtration rates did not change with the renal arterial pressure changes in these groups. In the group D dogs, during the larger pressure reductions of 54 ± 6.6 mm Hg from higher values of 158 ± 7.0 mm Hg, mean urine flow and effective renal blood flow remained constant while glomerular filtration rate and sodium output decreased only slightly. Output efficiency ratios related to perfusion pressure were calculated. With no more than modest pressure-induced excretory changes, it is concluded that excretory sodium and urinary volume autoregulation in concert with nearly perfect circulatory autoregulation were demonstrated with regionally varied mean renal arterial pressure. The same preglomerular myogenic responses to transvascular pressure, which restrict glomerular and transcapillary pressures, are viewed dominantly responsible for both circulatory and excretory autoregulation under normal conditions of minimal stress and low fractional sodium excretions. Homeostatic implications are discussed concerning likely relevance to the Guyton-Coleman theory for the long-term control of arterial blood pressure.

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Section: Discussionsupporting

confidence: 58%

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Waugh

1991

J Vasc Res

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“…The role of PG in attenuating the renal vasoconstriction induced by NE has been proposed in studies showing that 1) NE increases the production of PG in the kidney (6,15); 2) COX inhibition leads to a marked potentiation of NE-induced renal vasoconstriction (1,2,15); and 3) PG infusion attenuates the renal vasoconstriction elicited by NE (3,14). Some results reported in the aforementioned previous studies have been confirmed in our study, because we have found that intrarenal infusion of NE enhances the urinary excretion of PGE 2 and 6-keto-PGF 1␣ and that the renal hemodynamic effects of NE are potentiated by the infusion of a nonselective COX inhibitor.…”

Section: Discussionmentioning

confidence: 99%

“…renal function; glomerular filtration rate; renal vascular resistance; prostaglandins; cyclooxygenase-2 IT IS WELL KNOWN THAT ENDOGENOUS prostaglandins (PG) play an important role in regulating renal function when vasoconstrictor levels are elevated (1-3, 6, 14, 15, 18, 22). This notion is supported by studies showing that norepinephrine (NE) infusion induces an increment in renal synthesis of PG (5,15) and that the renal vasoconstriction induced by NE is significantly potentiated when synthesis of PG is reduced (1,2,15). Finally, it has been reported that PGI 2 infusion reduces the renal vasoconstriction elicited by NE (3,14).…”

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confidence: 89%

Role of COX-2-derived metabolites in regulation of the renal hemodynamic response to norepinephrine

Llinás

López

Rodríguez

et al. 2001

American Journal of Physiology-Renal Physiology

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Role of COX-2-derived metabolites in regulation of the renal hemodynamic response to norepinephrine. Am J Physiol Renal Physiol 281: F975-F982, 2001.-The objective of this study was to examine the role of cylcooxygenase (COX)-2-derived prostaglandins (PG) in modulating the renal hemodynamic effects of norepinephrine (NE) during low or normal sodium intake. The relative contribution of each COX isoform in producing the PG that attenuate the renal NE effects during normal sodium intake was also evaluated. The renal response to three doses of NE (50, 100, and 250 ng⅐kg Ϫ1 ⅐min Ϫ1) was evaluated in anesthetized dogs pretreated with vehicle, a selective COX-2 inhibitor (nimesulide), or a nonselective COX inhibitor (meclofenamate). Intrarenal infusion of the two lower doses of NE in vehicle-pretreated dogs with normal sodium intake (n ϭ 8) elicited an increase in renal vascular resistance (RVR; 21 and 34%) without inducing changes in glomerular filtration rate (GFR). The highest dose of NE in this group induced a further increment in RVR (113%) and a decrease in GFR (33%). Pretreatment with nimesulide in dogs with normal sodium intake (n ϭ 7) did not modify the NE-induced increments in RVR but enhanced the decreases in GFR induced by the three NE doses (12, 26, and 64%). The renal hemodynamic response to NE in meclofenamate-pretreated dogs with normal sodium intake (n ϭ 7) was similar to that found in dogs pretreated with nimesulide. Infusion of the lowest dose of NE to vehicle-pretreated dogs with low sodium intake (n ϭ 6) did not modify GFR and elicited an increase in RVR (42%). Infusion of the second and third doses of NE led to a decrease in GFR (35 and 91%) and a rise in RVR (82 and 587%). Infusion of the first two doses of NE in nimesulide-pretreated dogs with low sodium intake (n ϭ 5) induced a fall in GFR (64 and 92%) and an increase in RVR (174 and 2,293%) that were greater (P Ͻ 0.05) than those induced by NE in vehicle-pretreated dogs. The elevation in the urinary excretion rates of PGE 2 and 6-keto-PGF1␣ elicited by NE was prevented in the nimesulide-pretreated dogs. Our results show that COX-2 inhibition potentiates the renal hemodynamic effects of NE and propose that the PG involved in modulating them are mainly derived from COX-2 activity. renal function; glomerular filtration rate; renal vascular resistance; prostaglandins; cyclooxygenase-2 IT IS WELL KNOWN THAT ENDOGENOUS prostaglandins (PG) play an important role in regulating renal function when vasoconstrictor levels are elevated (1-3, 6, 14, 15, 18, 22). This notion is supported by studies showing that norepinephrine (NE) infusion induces an increment in renal synthesis of PG (5, 15) and that the renal vasoconstriction induced by NE is significantly potentiated when synthesis of PG is reduced (1, 2, 15). Finally, it has been reported that PGI 2 infusion reduces the renal vasoconstriction elicited by NE (3,14).Several studies have shown that both cyclooxygenase (COX) isoforms are constitutively expressed in the kidney and that the intrarenal loc...

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“…This appears to be a compensatory phenomenon in low-flow vasoconstrictive states such as hypovolemic shock, as shown by previous studies in our laboratory [2], in which higher plasma levels of histamine were dem onstrated in surviving than in nonsurviving animals. Ischemia of single organs is also associated with the release of histamine [3,4].…”

Section: Introductionmentioning

confidence: 99%

Oxygen Free Radical-Induced Histamine Release during Intestinal Ischemia and Reperfusion

1989

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Acute mesenteric ischemia is highly lethal and therefore a serious problem for surgery and intensive care medicine; accordingly its pathophysiology warrants further study. Oxygen free radicals (OFR) play a role in the intestinal mucosal damage that develops during reperfusion after ischemia. Histamine (H) is generally released in various types of tissue ischemia. The link between H release and OFR has only been studied in in vitro systems. We tested the hypothesis that OFR may be involved in H release following reperfusion of the ischemic gut. The artery supplying a segment of the ileum was occluded for 1 or 2 h in anesthetized dogs. On reperfusion, a release of H into the venous effluent of the segment was demonstrated. Pretreatment of the animals with allopurinol (an inhibitor of xanthine oxidase), or with MTDQ-DA [6,6’-methylenebis(2,2-dimethyl-4-methanesulfonic acid sodium-1,2-dihydroquinoline)], a superoxide anion scavenger, or with a combination of allopurinol and MTDQ-DA resulted in an inhibition of H release. We conclude that OFR may play a role in the local H release following intestinal ischemia.

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Vasoconstrictor-induced changes in renal blood flow: role of prostaglandins and histamine

Cited by 8 publications

References 0 publications

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Modest Pressure Natriuresis and Autoregulation during Water Diuresis in Dogs

Role of COX-2-derived metabolites in regulation of the renal hemodynamic response to norepinephrine

Oxygen Free Radical-Induced Histamine Release during Intestinal Ischemia and Reperfusion

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