GLOMERULAR HEMODYNAMICS and HORMONAL EVALUATION DURING STARVATION in RATS
Boim, Mirian Aparecida
Ramos, Oswaldo L.
Schor, Nestor [UNIFESP]
Is part ofKidney International
MetadataShow full item record
The effects of total food deprivation on renal function were evaluated in normal Munich-Wistar rats submitted to starvation (S) periods of two to eight days (Groups S2 to S8). A prompt and sustained decrease in renal plasma flow (RPF) and an increase in total renal vascular resistance (TRVR) were observed after the second day, together with a gradual decrease in glomerular filtration rate (GFR) until the fourth day (40% in the S4 group, P < 0.05). After this period, a spontaneous and progressive increase in GFR occurred in spite of continuing low RPF and high TRVR. Glomerular hemodynamics were evaluated in additional animals from groups S4 and S7. As observed for whole kidney GFR, mean single nephron (SN) GFR was reduced in group S4, but not in group S7. the decline in SNGFR in S4 was the result of a decline (approximately 40%) in glomerular plasma flow rate (Q(A)) and glomerular capillary hydraulic pressure (P(GC)), due to a predominant increase (approximately 60%) in afferent arteriolar resistance. in S7, SNGFR and its determinants did not differ from the control. Angiotensin II (Ang II), prostanglandin (but not thromboxane A2, TxA2) inhibition blunted the alterations in whole kidney function observed in S4. Conversely in S7, the inhibition of vasoconstrictor agents (Ang II and TxA2) did not normalize GFR, suggesting that the intrarenal vasoconstriction could be an important factor to maintain GFR after a prolonged period of starvation. Thus, prolonged starvation induces a biphasic profile of renal function in rats: a first phase characterized by a decline in GFR and SNGFR followed by an adaptative phase with normalization of GFR and superficial glomerular function. Results suggest that these physiological alterations are dependent on a complex hormonal relationship involving hormones such as Ang II and prostaglandins.
CitationKidney International. Malden: Blackwell Science Inc, v. 42, n. 3, p. 567-572, 1992.
- Em verificação - Geral