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P A de Vries

Publications and source records attributed to P A de Vries.

11 recordsLinked to original sources
PubMed1999

Impaired renal vascular response to a D1-like receptor agonist but not to an ACE inhibitor in conscious spontaneously hypertensive rats.

The natriuretic response to a dopamine 1-like receptor agonist is blunted in spontaneously hypertensive rats (SHRs). Whether the renal vasodilator response to D1-like receptor stimulation in SHRs is defective also is unclear. To determine whether the renal hemodynamic response to a D1-like receptor is impaired in SHR, we examined the effect of a continuous infusion of the D1-like receptor agonist fenoldopam (2 microg/kg/min) on systemic and renal hemodynamics in conscious SHRs and Wistar-Kyoto (WKY) rats. As an active control, we used an equivalent antihypertensive dosage of captopril (10 mg/kg). Fenoldopam significantly increased effective renal plasma flow (ERPF) in WKY rats (+22 +/- 5%; p < 0.01), whereas this response was absent in SHRs (+7 +/- 3%; NS). Mean arterial pressure (MAP) was significantly reduced in SHRs (-11 +/- 2%; p < 0.001), demonstrating a systemic vasodilator response to fenoldopam in SHRs. The reduction in renal vascular resistance (RVR) was more pronounced in WKY rats (-24 +/- 2%) than in SHRs (-13 +/- 4%; p < 0.05). Captopril significantly increased ERPF in SHRs (+16 +/- 3%; p < 0.001), demonstrating a preserved renal vasodilatory capacity in SHRs. The blunting of the renal vasodilatory response to fenoldopam in SHRs is present during a high as well as a low sodium intake. In conscious SHRs, the renal vasodilatory response to a D1-like receptor agonist is impaired, whereas the blood pressure response is more pronounced. The preserved renal vasodilatory response to captopril indicates that the defective vasodilatory response in SHRs is functional rather than due to altered structural properties of the renal vascular bed.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1998

Can continuous intraperitoneal infusion of 125I-iothalamate and 131I-hippuran be used for measurement of GFR in conscious rats?

We previously described a method to measure GFR in conscious spontaneously voiding rats. This method circumvents the need for anesthesia and for bladder instrumentation. It's main principle is the correction of renal 125I-iothalamate clearance for incomplete urine collection by the ratio of plasma and renal clearance of co-infused 131I-Hippuran. A disadvantage of this technique is the requirement of an intra-arterial catheter for infusion of the renal function tracers. We therefore tested whether intraperitoneal infusion of 125I-iothalamate and 131I-Hippuran can be used for such a GFR measurement in conscious spontaneously voiding rats. We found that during intraperitoneal administration, stable plasma levels of 131I-Hippuran could be obtained. However, urinary recovery of 131I-Hippuran was incomplete (66 +/- 32%), leading to a significant overestimation of GFR by 140 +/- 13% in comparison with the GFR measured by the intra-arterial technique. Thus intraperitoneal infusion of renal function tracers cannot replace intra-arterial infusion.

Animals↗
PubMed1992

Pyloric stenosis in a premature infant.

Workup of a case of hypertrophic pyloric stenosis in a premature infant showed absence of ultrasonic criteria for diagnosis. Transpyloric intubation for enteral feeding may delay the diagnosis of this disorder and has been thought to play a role in its development.

Humans↗
PubMed1978

[Not Available].

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Contraception↗
PubMedDate not supplied

Potentials and limitations of the low-molecular-weight protein lysozyme as a carrier for renal drug targeting.

Selective targeting of drugs to the kidney may enable an increased renal effectiveness combined with a reduction of extrarenal toxicity. Intrarenal delivery to the proximal tubular cell can be achieved using low-molecular-weight proteins, such as lysozyme. Administration of high dosages of lysozyme, required to study the effects of such conjugates in vivo, however, is restricted since a partial escape of the renal reabsorption and the occurrence of unwanted effects on systemic blood pressure and renal function may occur. The purpose of this study was to investigate the optimal parenteral administration schedule and the maximum dose of lysozyme, providing the most optimal tubular reabsorption and at the same time a minimal effect on blood pressure and renal hemodynamics, comparing continuous infusion of lysozyme with single dose injections. Urinary lysozyme excretion increased dose-dependently, both during continuous infusion and intravenous bolus injections. However, this loss of intact lysozyme into the urine was much higher after 3 injections of in total 250 mg x kg(-1) x 6 h(-1) (51.8+/-3.7% of the dose) compared to the same dose administered by continuous infusion (11.7+/-2.4%, P < 0.001). Continuous infusion of lysozyme up to 1000 mg x kg(-1) in 6 hours had no effect on systemic blood pressure, whereas a bolus injection of lysozyme (167 mg x kg(-1)) resulted in reversible blood pressure lowering of 52.2+/-2.2% (P<0.001). A dose-dependent decline of the glomerular filtration rate was observed at dosages of lysozyme higher than 100 mg x kg(-1) x 6 h(-1), with a maximal reduction of 53.0+/-3.7% after infusion of 1000 mg x kg(-1) x 6 h(-1). Effective renal plasma flow was less affected and only lowered statistically significant at dosages of 500 (-12.6+/-3.3%, P<0.05) to 1000 mg x kg(-1) x 6 h(-1) (-17.2+/-3.9%, P<0.01). We conclude that bolus injections of lysozyme should not be used for renal targeting purposes since it results in considerable tubular loss of lysozyme in the urine as well as cardiovascular side effects. In contrast, continuous infusion of lysozyme using dosages sufficient for renal drug targeting (maximally 15 mg x kg(-1) x h(-1)) only has minimal effects on blood pressure and renal hemodynamics, with a minimal urinary lysozyme loss as well.

Animals↗