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A P Provoost - One of the best experts on this subject based on the ideXlab platform.

  • renal vascular dysfunction precedes the development of renal damage in the hypertensive fawn Hooded Rat
    American Journal of Physiology-renal Physiology, 2010
    Co-Authors: Peter Ochodnický, A P Provoost, Robert H Henning, Hendrik Buikema, Dick De Zeeuw, Richard P E Van Dokkum
    Abstract:

    It is unknown whether generalized vascular dysfunction precedes the development of kidney disease. Therefore, we studied myogenic constriction and endothelium-mediated dilatory responses in two inb...

  • altered renal hemodynamics and impaired myogenic responses in the fawn Hooded Rat
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1999
    Co-Authors: Richard P E Van Dokkum, A P Provoost, Howard J Jacob, Chengwen Sun, Richard J. Roman
    Abstract:

    The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contribu...

  • tubuloglomerular feedback and prolonged ace inhibitor treatment in the hypertensive fawn Hooded Rat
    Nephrology Dialysis Transplantation, 1998
    Co-Authors: Gaico H Verseput, A P Provoost, Branko Braam, H A Koomans
    Abstract:

    Background. The spontaneously hypertensive fawn-Hooded (FHH) Rat develops severe glomerulosclerosis with ageing. The afferent arteriolar resistance is low, resulting in a strongly elevated glomerular capillary pressure (P GC ). Methods. Afferent arteriolar resistance is under the control of the tubuloglomerular feedback (TGF) system, and we studied whether young FHH Rats, i.e. at a stage when only mild glomerulosclerosis was present, have diminished TGF responsiveness. Results. Maximum TGF-mediated decreases in stop-flow pressure in response to late proximal perfusion with artificial tubular fluid were 9.0 ± 1.0 mmHg, a value not different or even slightly lower than observed in normal Rats. P GC was 59.9 ± 1.2 mmHg and the estimated P GC at half-maximal activation of the TGF system (opeRating P GC ) was 54.5±0.8 mmHg at 11 weeks of age (n = 11), a value higher than observed in normal Rats. The second question of the present study concerns the effect of chronic angiotensin-I-converting enzyme inhibitor (ACE-i) administRation on P GC . ACE-i, by reducing angiotensin II (Ang II) availability, diminishes TGF responsiveness, which would offset the beneficial effect on P GC under normal flow conditions to the macula densa. Maximum TGF responses were 8.9 ± 1.0 and 17.5 ± 1.5 mmHg in 11- and 26-week-old Rats that had been treated with the ACE-i lisinopril in the drinking water started when the animals were 7 weeks of age. P GC was 44.3 ± 1.2 (n = 9) and opeRating P GC was 40.1 ± 1.6 mmHg (n=9) at 11, values significantly lower than in untreated Rats. Values remained lower in the 26-week-old treated animals and were 40.9 ± 0.8 and 32.6 ± 1.1 mmHg. Conclusions. (1) the TGF system in this model of spontaneous hypertension and glomerulosclerosis is intact, despite the fact that the FHH Rat has a characteristically low afferent arteriolar resistance as compared to other hypertensive Rats; (2) the Rat displays a normal or even enhanced function of the TGF system following prolonged administRation of the ACE-i lisinopril. The latter finding indicates that the reduction of P GC achieved by the ACE-i is not offset by a concomitant attenuation of TGF function.

  • angiotensin converting enzyme inhibition in the prevention and treatment of chronic renal damage in the hypertensive fawn Hooded Rat
    Journal of The American Society of Nephrology, 1997
    Co-Authors: G H Verseput, A P Provoost, B B Braam, Jan J Weening, H A Koomans
    Abstract:

    The spontaneously hypertensive fawn-Hooded Rat (FHH) develops acceleRated albuminuria and focal glomerular sclerosis (FGS), leading to ESRD and shortening of lifespan. The FHH is characterized by modeRate systemic hypertension, a relatively low afferent to efferent arteriolar resistance Ratio, and glomerular hypertension. The FHH study presented here was designed to examine the efficacy of early-onset, late-onset, or early-temporary angiotensin I-converting enzyme inhibition (ACE-i) in amelioRating long-term hypertension and FGS, and improving survival, as well as to relate its protective efficacy to preexistent FGS and to reduction of glomerular pressure (PGC) Untreated Rats developed hypertension and high PGC, and all (N = 22) except one died of ESRD within the 72-wk follow-up period. Early-onset (at 7 wk of age) ACE-i prevented development of systemic and glomerular hypertension, and it largely prevented proteinuria and FGS; all Rats survived throughout the follow-up period. Rats treated with late-onset (22 wk) ACE-i were hypertensive and proteinuric at the start of ACE-i, and they showed beginning FGS. ACE-i corrected the hypertension, albuminuria, and PGC but could not fully prevent some hypertension, albuminuria, and FGS at the later stage. Early-temporary (7 to 22 wk) ACE-i adequately controlled blood pressure and development of FGS during therapy, but after withdrawal of ACE-i, systemic and glomerular hypertension developed as in untreated animals. This regimen postponed but did not control FGS development and early mortality. The results of this study indicate that: (1) early-onset ACE-i very effectively protects against development of renal damage in the FHH; (2) this protection is associated with normalization of the elevated glomerular capillary pressure; (3) ACE-i cannot completely prevent further development of previously established FGS, despite lowering glomerular capillary pressure; (4) early-temporary ACE-i has no long-term controlling effect on arterial and glomerular pressure, and it cannot control development of FGS.

  • renal disease susceptibility and hypertension are under independent genetic control in the fawn Hooded Rat
    Nature Genetics, 1996
    Co-Authors: Donna M Brown, A P Provoost, Mark J Daly, Eric S Lander, Howard J Jacob
    Abstract:

    Hypertension, diabetes and hyperlipidemia are risk factors for life-threatening complications such as end-stage renal disease, coronary artery disease and stroke. Why some patients develop complications is unclear, but only susceptibility genes may be involved. To test this notion, we studied crosses involving the fawn-Hooded Rat, an animal model of hypertension that develops chronic renal failure. Here, we report the localization of two genes, Rf-1 and Rf-2, responsible for about half of the genetic variation in key indices of renal impairment. In addition, we localize a gene, Bpfh-1, responsible for about 26% of the genetic variation in blood pressure. Rf-1 strongly affects the risk of renal impairment, but has no significant effect on blood pressure. Our results show that susceptibility to a complication of hypertension is under at least partially independent genetic control from susceptibility to hypertension itself.

Richard P E Van Dokkum - One of the best experts on this subject based on the ideXlab platform.

  • renal myogenic constriction protects the kidney from age related hypertensive renal damage in the fawn Hooded Rat
    Journal of Hypertension, 2013
    Co-Authors: Peter Vavrinec, Robert H Henning, Maaike Goris, Sjoerd W Landheer, Hendrik Buikema, Richard P E Van Dokkum
    Abstract:

    Introduction:Intact myogenic constriction plays a role in renal blood flow autoregulation and protection against pressure-related (renal) injury. However, to what extent alteRations in renal artery myogenic constriction are involved in development of renal damage during aging is unknown. Therefore, we studied two strains of fawn-Hooded Rats, which differ in expression of hypertension and chronic renal failure.Methods:Ten-week-old fawn-Hooded hypertensive (FHH) and fawn-Hooded low blood pressure (FHL) Rats were followed for SBP and proteinuria for 1 year. At 52 weeks of age, the kidney was removed and studied for focal glomerulosclerosis (FGS) and glomerular cross-sectional area, and myogenic constriction of isolated small renal arteries in a vessel perfusion set up. Renal myogenic constriction and FGS were additionally determined in 10-week-old fawn-Hooded Rats.Results:At young age, fawn-Hooded Rats did not differ in SBP, FGS, and urinary protein excretion, but renal artery myogenic constriction already was significantly smaller (approximate to 50%) in FHH compared with FHL Rats. Aging in fawn-Hooded Rats was associated with increase in SBP and urinary protein excretion and loss of renal artery myogenic constriction. These changes occurred in both fawn-Hooded strains, although that in FHH Rats the onset of hypertension occurred earlier and the increase in proteinuria by far exceeded (>4 times) that observed in FHL Rats, and came along with 5.5 times increase in FGS and 1.3 times increase in glomerular cross-sectional area and significantly less preserved renal artery myogenic constriction in FHH Rats.Conclusion:Better preservation of renal myogenic constriction protects the kidney from age-related hypertensive renal damage in the fawn-Hooded Rat.

  • renal vascular dysfunction precedes the development of renal damage in the hypertensive fawn Hooded Rat
    American Journal of Physiology-renal Physiology, 2010
    Co-Authors: Peter Ochodnický, A P Provoost, Robert H Henning, Hendrik Buikema, Dick De Zeeuw, Richard P E Van Dokkum
    Abstract:

    It is unknown whether generalized vascular dysfunction precedes the development of kidney disease. Therefore, we studied myogenic constriction and endothelium-mediated dilatory responses in two inb...

  • altered renal hemodynamics and impaired myogenic responses in the fawn Hooded Rat
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1999
    Co-Authors: Richard P E Van Dokkum, A P Provoost, Howard J Jacob, Chengwen Sun, Richard J. Roman
    Abstract:

    The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contribu...

  • Impaired autoregulation of renal blood flow in the fawn-Hooded Rat
    The American journal of physiology, 1999
    Co-Authors: Richard P E Van Dokkum, Abraham P. Provoost, Howard J Jacob, Magdalena Alonso-galicia, Richard J. Roman
    Abstract:

    The responses to changes in renal perfusion pressure (RPP) were compared in 12-wk-old fawn-Hooded hypertensive (FHH), fawn-Hooded low blood pressure (FHL), and August Copenhagen Irish (ACI) Rats to...

Steven H Abman - One of the best experts on this subject based on the ideXlab platform.

  • abnormal lung growth and the development of pulmonary hypertension in the fawn Hooded Rat
    American Journal of Physiology-lung Cellular and Molecular Physiology, 1999
    Co-Authors: Timothy D. Le Cras, Dug-ha Kim, Neil E. Markham, Sarah A Gebb, John M Shannon, Rubin M Tuder, Steven H Abman
    Abstract:

    The Fawn-Hooded Rat (FHR) strain develops acceleRated and severe pulmonary hypertension when exposed to slight decreases in alveolar P O 2 . We recently observed that adult FHR lungs showed a strik...

  • matuRational changes in lung endothelin 1 expression in the fawn Hooded Rat during the development of pulmonary hypertension
    Pediatric Research, 1999
    Co-Authors: Conrad L Epting, Timothy D. Le Cras, Neil E. Markham, Gresham T Richter, Steven H Abman
    Abstract:

    MatuRational Changes in Lung Endothelin-1 Expression in the Fawn Hooded Rat during the Development of Pulmonary Hypertension

  • impaired developmental expression of lung endothelial nitric oxide synthase and abnormal alveolarization in the fawn Hooded Rat implications for the risk of developing pulmonary hypertension 1689
    Pediatric Research, 1998
    Co-Authors: Dug-ha Kim, Timothy D. Le Cras, Rubin M Tuder, Marilee P Horan, Steven H Abman
    Abstract:

    The fawn-Hooded Rat (FHR) strain is characterized by platelet abnormalities and systemic hypertension, and has been used to study genetic risk factors for pulmonary hypertension (PH). Unlike other strains, FHR develop progressive PH when exposed to slight decreases in alveolar PaO2. We hypothesized that developmental abnormalities in lung vasoreactivity or growth may predispose the FHR for PH. Since endogenous nitric oxide (NO) modulates pulmonary vasoreactivity and growth, we further hypothesized that early decreases in lung endothelial NO synthase (eNOS) content may contribute to the development of PH in FHR. We measured lung eNOS content and growth in FHR and control Rat strains (Fischer and Sprague-Dawley (SDR)). Lungs were harvested from late fetal and postnatal ages (days 1 & 7) and eNOS protein content measured by western blot analysis. Immunostaining for eNOS was performed with paraffin sections and the eNOS monoclonal antibody. Histology was assessed after tracheal installation of formalin at constant pressure (10cm water) and radial alveolar counts performed. Lung to body weight Ratios were reduced in fetal and newborn FHR by 20-46% compared to controls (p<0.05). In comparison with SDR, FHR lung eNOS protein was decreased to 69±8%, 56±8%, and 68±7% at fetal, and postnatal days 1 and 7, respectively (p<0.05 at each age). Immunostaining studies demonstRated selective staining for eNOS only in vascular endothelium and no difference in the pattern of eNOS expression between strains. Histology revealed striking changes in lung matuRation and growth in FHR at all ages, including reduced alveolarization(FHR 58±2% of SDR at day 7, p<0.05). We conclude that in comparison with other Rat strains, lung eNOS content is decreased in the FHR fetus and newborn. In addition, the FHR lung has decreased alveolarization and histologic signs of delayed lung matuRation. We speculate that reduced vascular surface area and eNOS increase the risk for developing PH, and that decreased NO production may be associated with abnormal lung growth and development.

Howard J Jacob - One of the best experts on this subject based on the ideXlab platform.

Andrew J Lawrence - One of the best experts on this subject based on the ideXlab platform.

  • the effect of chronic ethanol consumption and withdrawal on μ opioid and dopamine d1 and d2 receptor density in fawn Hooded Rat brain
    Journal of Pharmacology and Experimental Therapeutics, 2002
    Co-Authors: Elvan Djouma, Andrew J Lawrence
    Abstract:

    Previous studies have implicated the dopamine and opioid systems in the induction and maintenance of ethanol consumption. This study investigated, in alcohol-preferring Fawn-Hooded (FH) Rats, whether chronic free-choice ethanol consumption and subsequent withdrawal cause alteRations in central mu-opioid, dopamine D(1), and D(2) receptor density using autoradiography. FH Rats were given a free choice between a 5% ethanol solution and tap water (n = 25) and displayed a mean ethanol consumption of 5.6 g/kg/day. A parallel group of FH Rats (n = 5) only had access to tap water. Rats were then withdrawn from ethanol for 0, 1, 2, 5, or 10 days and killed by cervical dislocation and decapitation. Increases in mu-opioid receptor density were observed in the nucleus accumbens and ventral tegmental area upon withdrawal compared with the ethanol naive group. In the lateral amygdala, binding in all withdrawal groups was significantly different from the ethanol naive FH Rats, and also from the chronic ethanol Rats. An increase in dopamine D(1) receptor density was observed in the substantia nigra, pars reticulata in the 5- and 10-day withdrawal groups compared with ethanol naive. Accumbal dopamine D(2) receptor density (+25-30%) increased in the 10-day withdrawal group compared with both naive and chronic ethanol groups. These findings demonstRate that the opioid and dopamine systems are susceptible to modulation by chronic ethanol consumption and withdrawal in the FH Rat. Furthermore, although acute ethanol withdrawal results in modulation of mu-opioid receptors, effects on dopamine receptors are delayed and only become evident 5 to 10 days after withdrawal.

  • compaRative analysis of the central cck system in fawn Hooded and wistar kyoto Rats extended localisation of cck a receptors throughout the Rat brain using a novel radioligand
    Regulatory Peptides, 2001
    Co-Authors: Daniel J Lodge, Andrew J Lawrence
    Abstract:

    Abstract The neuropeptide cholecystokinin has been implicated in the actions of a number of central processes including anxiety and reward. For this reason, the aim of the present study was to compare the density of CCK-A and -B receptors and the mRNA encoding preproCCK throughout the brains of an alcohol-preferring (Fawn Hooded) Rat strain with that of a non-alcohol-preferring (Wistar Kyoto) strain of Rat. Our study revealed significant differences with regard to the central CCK system of the FH compared to the WKY Rat, including differences in CCK-A receptor binding throughout the dorsal medulla, and altered CCK-B binding density throughout the cerebral cortex and reticular nucleus of the thalamus. The most striking result, given the altered behavioural phenotype of the FH Rat, was the 33% lower density of CCKmRNA measured throughout the ventral tegmental area of the FH Rat when compared to the WKY. This study also reports on a protocol to utilise a novel radioligand, [ 125 I]- d -Tyr-Gly-A-71378, for autoradiographic detection of CCK-A receptors throughout the Rat brain. As previously reported, CCK-A receptors were located throughout the area postrema, interpeduncular nucleus and nucleus tractus solitarii; however, binding to CCK-A receptors was also visualised throughout the medial pre-optic area, the arcuate nucleus and the circumventricular regions of the ventral hypothalamus, regions known to contain CCK-A receptors but which were previously undetectable using autoradiography in Rat brain.

  • up regulation of cortical ampa receptor binding in the fawn Hooded Rat following ethanol withdrawal
    European Journal of Pharmacology, 1999
    Co-Authors: Feng Chen, Bevyn Jarrott, Andrew J Lawrence
    Abstract:

    Abstract The present study has employed quantitative receptor autoradiography to compare the binding of (S)-[3H]5-fluorowillardiine to (S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors in the brains of alcohol-preferring Fawn-Hooded (FH) Rats, alcohol non-preferring Wistar–Kyoto (WKY) Rats, and FH Rats following a 28-day period of 5% ethanol consumption with or without ethanol withdrawal. Significantly higher binding of [3H]5-fluorowillardiine was found in the cingulate cortex (+12%) and claustrum (+13%) in alcohol naive FH Rats compared to WKY Rats. Chronic ethanol consumption decreased binding of (S)-[3H]5-fluorowillardiine in four cortical regions (frontal, parietal, occipital and temporal cortex), hippocampus and septohippocampal nucleus. In contrast, ethanol withdrawal induced a significant “rebound” increase in binding by +22% in frontal and parietal cortex, by +17% in cingulate cortex and +13% in claustrum, and by +14% in the septohippocampal nucleus compared to chronic ethanol-exposed FH Rats. The findings suggest that AMPA receptors in frontal cortical regions are sensitive to ethanol and therefore may be implicated in the predisposition of alcohol preference in FH Rats.