Effect of a serotonin blocking agent on renal hemodynamics in the normal rat

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat. These studies were designed to explore the effects of ketanserin (K), a serotonergic S2-receptor blocker on glomerular filtration rate (GFR), renal plasma flow (RPF) and autoregulation of renal blood flow (RBF) in the normal, anesthetized rat. Two doses of ketanserin were used: a high dose that, in addition to its serotonin blocking effect, possessed alpha 1-adrenergic blocking capacities; and a low dose that acted only as a serotonin S2 blocking agent. The effects of the high dose were compared to the effects of phenotolamine. Both the high dose of K and phentolamine resulted in a similar fall of systemic blood pressure from 117 ± 4 to 78 ± 3 and from 121 ± 4.5 to 76 ± 5mm Hg, respectively (P < 0.01). Despite this fall, GFR and RPF remained unchanged from 2.36 ± 0.16 ± to 2.26 ± 0.12 ml/min, and from 5.33 ± 0.41 to 5.76 ± 0.5ml/min with K, while both parameters significantly decreased with phentolamine. A remarkable preservation of the autoregulation of RBF until a renal perfusion pressure (RPP) of 70 to 75mm Hg was noted with K, but not with phentolamine or Ringer infusion. With the low dose of K, a significant rise in GFR and PAH clearance was noted, from 2.12 ± 0.17 to 2.59 ± 0.18 and from 4.81 ± 0.35 to 5.66 ± 0.48 ml/min, respectively (P < 0.05). A similar preservation of autoregulation of RBF was observed. Our studies suggest that in the pressure ranges below normal autoregulation of RBF in the rat, serotonin blockade is associated with maintenance of both GFR and RBF

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat

Effect of a serotonin blocking agent on renal hemodynamics in the normal rat. These studies were designed to explore the effects of ketanserin (K), a serotonergic S2-receptor blocker on glomerular filtration rate (GFR), renal plasma flow (RPF) and autoregulation of renal blood flow (RBF) in the normal, anesthetized rat. Two doses of ketanserin were used: a high dose that, in addition to its serotonin blocking effect, possessed alpha 1-adrenergic blocking capacities; and a low dose that acted only as a serotonin S2 blocking agent. The effects of the high dose were compared to the effects of phenotolamine. Both the high dose of K and phentolamine resulted in a similar fall of systemic blood pressure from 117 ± 4 to 78 ± 3 and from 121 ± 4.5 to 76 ± 5mm Hg, respectively (P < 0.01). Despite this fall, GFR and RPF remained unchanged from 2.36 ± 0.16 ± to 2.26 ± 0.12 ml/min, and from 5.33 ± 0.41 to 5.76 ± 0.5ml/min with K, while both parameters significantly decreased with phentolamine. A remarkable preservation of the autoregulation of RBF until a renal perfusion pressure (RPP) of 70 to 75mm Hg was noted with K, but not with phentolamine or Ringer infusion. With the low dose of K, a significant rise in GFR and PAH clearance was noted, from 2.12 ± 0.17 to 2.59 ± 0.18 and from 4.81 ± 0.35 to 5.66 ± 0.48 ml/min, respectively (P < 0.05). A similar preservation of autoregulation of RBF was observed. Our studies suggest that in the pressure ranges below normal autoregulation of RBF in the rat, serotonin blockade is associated with maintenance of both GFR and RBF

Controversies in acute kidney injury: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) conference

In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) published a guideline on the classification and management of acute kidney injury (AKI). The guideline was derived from evidence available through February 2011. Since then, new evidence has emerged that has important implications for clinical practice in diagnosing and managing AKI. In April of 2019, KDIGO held a controversies conference entitled Acute Kidney Injury with the following goals: determine best practices and areas of uncertainty in treating AKI; review key relevant literature published since the 2012 KDIGO AKI guideline; address ongoing controversial issues; identify new topics or issues to be revisited for the next iteration of the KDIGO AKI guideline; and outline research needed to improve AKI management. Here, we present the findings of this conference and describe key areas that future guidelines may address

The influence of renal replacement therapy on cardiac disease in the patiënt with endstage renal disease.

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