Tubuloglomerular feedback and prolonged ACE-inhibitor treatment in the hypertensive fawn-hooded rat
| Autor: | Branko Braam, Hendrik A. Koomans, Gaico H. Verseput, Abraham P. Provoost |
|---|---|
| Přispěvatelé: | Pediatric Surgery |
| Rok vydání: | 1998 |
| Předmět: |
Male
medicine.medical_specialty Renal glomerulus Kidney Glomerulus Angiotensin-Converting Enzyme Inhibitors Feedback Internal medicine Renin–angiotensin system medicine Animals Tubuloglomerular feedback Transplantation business.industry Angiotensin II Lisinopril Glomerulosclerosis medicine.disease Rats Kidney Tubules medicine.anatomical_structure Endocrinology Nephrology Hypertension ACE inhibitor Macula densa business medicine.drug |
| Zdroj: | Nephrology Dialysis Transplantation, 13, 893-899. Oxford University Press |
| ISSN: | 0931-0509 |
| DOI: | 10.1093/ndt/13.4.893 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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