Missale, Cristina, S. Russel Nash, Susan W. Robinson, Mohamed Jaber, and Marc G. Caron. Dopamine Receptors: From Structure to Function. Physiol. Rev. 78: 189–225, 1998. — The diverse physiological actions of dopamine are mediated by at least five distinct G protein-coupled receptor subtypes. Two D1-like receptor subtypes (D1 and D5) couple to the G protein Gs and activate adenylyl cyclase. The other receptor subtypes belong to the D2-like subfamily (D2 , D3 , and D4) and are prototypic of G protein-coupled receptors that inhibit adenylyl cyclase and activate K+ channels. The genes for the D1 and D5 receptors are intronless, but pseudogenes of the D5 exist. The D2 and D3 receptors vary in certain tissues and species as a result of alternative splicing, and the human D4 receptor gene exhibits extensive polymorphic variation. In the central nervous system, dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion, and affect as well as neuroendocrine s...

Dopamine Receptors: From Structure to Function

Background— In patients undergoing percutaneous coronary intervention (PCI) in the modern era, the incidence and prognostic implications of acute renal failure (ARF) are unknown. Methods and Results— With a retrospective analysis of the Mayo Clinic PCI registry, we determined the incidence of, risk factors for, and prognostic implications of ARF (defined as an increase in serum creatinine [Cr] >0.5 mg/dL from baseline) after PCI. Of 7586 patients, 254 (3.3%) experienced ARF. Among patients with baseline Cr 2.0, all had a significant risk of ARF. In multivariate analysis, ARF was associated with baseline serum Cr, acute myocardial infarction, shock, and volume of contrast medium administered. Twenty-two percent of patients with ARF died during the index hospitalization compared with only 1.4% of patients without ARF (P<0.0001). After adjustment, ARF remained strongly associated with death. Amo...

/pdf/incidence-and-prognostic-importance-of-acute-renal-failure-45f2o93xb6.pdf

Incidence and Prognostic Importance of Acute Renal Failure After Percutaneous Coronary Intervention

Effects of problem-based learning: a meta- analysis

Importance of Venous Congestion for Worsening of Renal Function in Advanced Decompensated Heart Failure

The changing faces of glutathione, a cellular protagonist

Dietary phosphate intake is now recognized to be a primary regulator of renal phosphate excretion. However, the nephron sites involved in the adaptation to changes in dietary phosphate are unclear. We tested the hypothesis that deep and superficial nephrons respond differently to changes in dietary phosphate by comparing fractional phosphate delivery (FDP%) from proximal tubules of both nephron populations. Because phosphate reabsorption is not detectable in the ascending loop of Henle, FDP% to the superficial early distal tubule and papillary loop of Henle reflect delivery from superficial and deep nephron proximal tubules, respectively. Micropuncture experiments were performed in 17 acutely TPTX rats fed either a low (0.07%) or a high (1.8%) phosphate diet for 4 days prior to the experiment. In low phosphate diet, fractional phosphate excretion was 0.93 +/- 0.26%. FDP% was 7.5 +/- 0.5 and 9.1 +/- 2.2% from superficial and deep nephron proximal tubules, respectively (P greater than 0.05). In high phosphate diet, fractional phosphate excretion was 29.6 +/- 5.0%. FDP% was significantly greater from superficial proximal tubules, 33.9 +/- 4.6%, compared with that from deep nephron proximal tubules, 14.0 +/- 2.7% (P less than 0.05). We conclude that significant adaptation of phosphate reabsorption in response to changes in dietary phosphate intake occurs in the superficial but not in the deep nephron proximal tubule in acutely TPTX volume-expanded rats. In addition, the presence of distal phosphate reabsorption was not evident in high phosphate diet but must occur in low phosphate diet.

Adaptation of deep and superficial nephrons to changes in dietary phosphate intake

The objective of this study was to test the hypothesis that changes in renal perfusion pressure (RPP) are not fully transmitted to the renal interstitium in spontaneous hypertension in comparison with normotensive states. Okamoto spontaneously hypertensive and normotensive Wistar-Kyoto rats were used in this study. Renal interstitial hydrostatic pressure (RIHP) was measured directly and continuously via a polyethylene matrix that was implanted chronically in the left kidney 3 wk before RIHP measurement. When RPP was allowed to increase from 136 +/- 0.5 to 162 +/- 1.3 mmHg in male spontaneously hypertensive rats, RIHP was not significantly changed from 3.7 +/- 0.9 to 4.6 +/- 1.1 mmHg, and fractional excretion of sodium (FENa) increased significantly from 0.26 +/- 0.12 to 0.65 +/- 0.15% (P less than 0.05). When RPP was allowed to change from 104 +/- 0.9 to 127 +/- 1.3 mmHg in male Wistar-Kyoto rats, RIHP increased markedly from 4.0 +/- 0.3 to 7.2 +/- 0.4 mmHg (P less than 0.05), and FENa was significantly elevated from 0.27 +/- 0.08 to 2.02 +/- 0.55% (P less than 0.05). In conclusion, spontaneously hypertensive rats have a blunted increase in RIHP and pressure natriuresis response in comparison with Wistar-Kyoto rats. Thus, in Okamoto spontaneously hypertensive rats, the effect of RPP on RIHP is attenuated, leading to a blunted pressure natriuresis response.

Renal interstitial hydrostatic pressure during pressure natriuresis in hypertension.

Phosphate transport along the nephron

The newly discovered peptides extracted from cardiac atria, atrial natriuretic factors (ANFs), when administered parenterally cause renal hemodynamic changes and natriuresis The nephron sites and cellular mechanism accounting for profound increase in Na+ excretion in response to ANFs are not yet clarified In the present study we investigated whether synthetic ANF peptide alters the reabsorption of Na+ and reabsorption of solutes cotransported with Na+ in the proximal tubules of rats Synthetic ANF peptide consisting of 26 amino acids, 4 micrograms/kg body wt/h, or vehicle in controls, was infused to surgically thyroparathyroidectomized anesthetized rats After determination of the fractional excretion (FE) of electrolytes (Na+, K+, Pi, Ca2+, Mg2+, HCO3), the kidneys were removed and luminal brush border membrane vesicles (BBMVs) were prepared from renal cortex Solute transport was measured in BBMVs by rapid filtration techniques Infusion of ANF peptide increased FENa, FEPi, and FEHCO3; but FECa, FEK, and FEMg were not changed The increase in FENa was significantly correlated, on the one hand, with increase of FEPi (r = 09, n = 7; P less than 001) and with increase of FEHCO3 (r = 089, n = 7; P less than 001) On the other hand, FENa did not correlate with FEK, FECa, or with FEMg The Na+ gradient-dependent uptake of Pi by BBMVs prepared from renal cortex of rats receiving ANF infusion was significantly (P less than 005) decreased (-25%), whereas the Na+ gradient-dependent uptake of L-[3H]proline and of D-[3H]glucose or the diffusional uptake of 22Na+ were not changed ANF-elicited change in FEPi showed a close inverse correlation with decrease of Na+-dependent Pi uptake by BBMVs isolated from infused rats (r = 099, n = 7; P less than 0001) Direct addition of ANF to BBMVs in vitro did not change the Na+ gradient-dependent Pi uptake In rats infused with ANF, the rate of amiloride-sensitive Na+-H+ exchange across the brush border membrane (BBM) was significantly (P less than 005) decreased (-40%), whereas the diffusional 22Na+ uptake (05 min) and the equilibrium (120 min) uptake of 22Na+ were not changed The inhibition of Na+-H+ exchange after ANF was likely due to alteration of the BBM antiporter itself, in that the H+ conductance of BBMVs was not increased We conclude that synthetic ANF (a) decreases tubular Na+ reabsorption linked to reabsorption of HCO3 in proximal tubules, and (b) inhibits proximal tubular reabsorption of Pi coupled to Na+ reabsorption, independent of secretion and/or action of parathyroid hormone or calcitonin These ANF effects are associated with inhibition of Na+-Pi synport and of Na+-H+ antiport in luminal BBMs Our findings document that inhibition of Na+-coupled transport processes in proximal tubules is an integral part of the renal response to ANF

/pdf/administration-of-atrial-natriuretic-factor-inhibits-sodium-1tts7dgh38.pdf

Administration of atrial natriuretic factor inhibits sodium-coupled transport in proximal tubules.

Systemic inhibition of nitric oxide synthesis with NG-monomethyl-L-arginine (L-NMMA) increases renal perfusion pressure (RPP) and urinary sodium excretion. Increased RPP has been proposed as one of...

Role of renal interstitial hydrostatic pressure in natriuresis of systemic nitric oxide inhibition

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