The effect of two different calcium antagonists on the glomerular haemodynamics in the dog
Language English Country Germany Media print
Document type Journal Article
PubMed
2336352
DOI
10.1007/bf02584016
Knihovny.cz E-resources
- MeSH
- Calcium Channel Blockers pharmacology MeSH
- Vascular Resistance drug effects MeSH
- Kidney Glomerulus blood supply MeSH
- Hemodynamics drug effects MeSH
- Urine physiology MeSH
- Nifedipine pharmacology MeSH
- Osmolar Concentration MeSH
- Dogs MeSH
- Punctures MeSH
- Verapamil pharmacology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Dogs MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Calcium Channel Blockers MeSH
- Nifedipine MeSH
- Verapamil MeSH
Kidney function of beagles fed a constant amount of food containing 3 mmol sodium.kgbodywt-1.day-1, and anaesthetized with pentobarbitone was investigated by clearance and micropuncture techniques during an intrarenal infusion of saline or the calcium antagonists verapamil (VER, 4 micrograms.kgbodywt-1.min-1) or nifedipine (NIF, 0.3 microgram.kgbodywt-1.min-1). Neither drug changed the mean arterial pressure. Apart from the natriuresis and diuresis, which were significantly greater with NIF than with VER, the response to both drugs was similar. Increases in renal blood flow (RBF; 17% with VER, 20% with NIF), glomerular filtration rate (GFR; VER: 34%; NIF: 39%) and filtration fraction (VER: 12%; NIF: 14%) were observed; similar values were obtained at the single nephron level. Pressure in glomerular capillaries, measured directly after ablation of a thin layer of cortex corticis, was increased by 11% with VER and 10% with NIF; no changes in proximal tubular and peritubular capillary pressure were seen. The glomerular ultrafiltration coefficient (Kf) did not change with either drug. Total arteriolar resistance was decreased (VER: 20%; NIF: 15%) due to a decrease in afferent resistance (VER: 31%; NIF: 27%) with no corresponding change in efferent resistance. The cause of the lack of responsiveness of the efferent arteriole remains unclear. In conclusion, in acute experiments with intrarenal administration, both drugs increase RBF and GFR by a preferential afferent dilatory mechanism without any change in Kf.
See more in PubMed
Am J Physiol. 1983 Oct;245(4):E410-6 PubMed
Am J Physiol. 1970 Dec;219(6):1658-64 PubMed
Circ Res. 1986 Jun;58(6):874-81 PubMed
J Cardiovasc Pharmacol. 1986 May-Jun;8(3):636-40 PubMed
Am J Physiol. 1981 Jul;241(1):F77-84 PubMed
Proc Soc Exp Biol Med. 1985 Jun;179(2):201-5 PubMed
Kidney Int. 1981 Jan;19(1):15-23 PubMed
Kidney Int. 1984 Jun;25(6):857-68 PubMed
Pflugers Arch. 1980 Jun;385(3):253-8 PubMed
Kidney Int. 1979 Aug;16(2):137-47 PubMed
Am J Med. 1987 Mar 30;82(3B):23-8 PubMed
Ren Physiol. 1986;9(6):357-65 PubMed
Ren Physiol. 1984;7(6):329-43 PubMed
J Physiol. 1982 Sep;330:449-60 PubMed
Hypertension. 1983 Jul-Aug;5(4):482-8 PubMed
J Cardiovasc Pharmacol. 1988;12 Suppl 4:S1-5 PubMed
Ren Physiol. 1984;7(2):90-101 PubMed
Am J Cardiol. 1987 Jan 23;59(2):72A-75A PubMed
J Clin Invest. 1984 Nov;74(5):1830-41 PubMed
Kidney Int. 1984 Sep;26(3):263-8 PubMed
Kidney Int. 1983 Jun;23(6):794-806 PubMed
Circ Res. 1964 Aug;15:SUPPL:132-41 PubMed
Am J Physiol. 1984 Sep;247(3 Pt 2):F447-52 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1974;285(3):201-7 PubMed
Am J Physiol. 1987 Dec;253(6 Pt 2):F1157-63 PubMed
