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Biomedical subjects

S Yarimizu

Publications and source records attributed to S Yarimizu.

9 recordsLinked to original sources
PubMed1979

Feedback mediation of SNGFR autoregulation in hydropenic and DOCA- and salt-loaded rats.

Tubuloglomerular feedback (TGF) mediation of autoregulation was investigated by measuring the response of single nephron glomerular filtration rate (SNGFR) to changes in arterial pressure (AP) following acute or chronic TGF inhibition. In hydropenic rats with intact TGF, distal SNGFR was 25.0 +/- 1.2 (SE) and 23.9 +/- 1.4 nl/min at AP of 111 and 135 mmHg, respectively. In the same 20 nephrons during proximal tubular microinfusion of furosemide, distal SNGFR was 23.6 +/- 1.4 (n = 16) and 29.7 +/- 1.4 nl/min (n = 20) (P less than 0.001, n = 16) at 112 and 133 mmHg. When determined proximally, SNGFR was 25.6 +/- 1.0 and 29.5 +/- 0.9 nl/min (P less than 0.001, n = 31) at 112 and 157 mmHg; kidney GFR increased similarly. These data and the predictions of a GFR model were then used to estimate autoregulatory efficiency. This analysis indicated that partial autoregulation occurred during TGF inhibition. Therefore, TGF is an essential, but probably not the only, mechanism mediating SNGFR autoregulation.

Absorption↗
PubMed1978

Protective effect of propranolol in the treatment of ischemically damaged canine kidneys prior to transplantation.

Warm ischemia is a potential problem during the harvesting of cadaveric kidneys for transplantation purposes. This ischemia can cause impaired renal function following transplantation. The purpose of our study was to determine whether the beta-adrenergic blocking agent propranolol was effective in improving renal function after ischemia. Dog kidneys were subjected to 30 minutes of warm ischemia followed by hypothermic pulsatile preservation for 24 hours. The kidneys then were autotransplanted with immediate contralateral nephrectomy. In this model only 50% of the untreated control group survived. Three different protocols using propranolol were tested. Administration of propranolol to dogs before the ischemic period, or installation of propranolol into the renal artery at the start of the ischemia, or addition of propranolol to the preservation perfusate lessened the severity of acute tubular necrosis and resulted in 100% long-term survival. Although the mechanism was not investigated, it has been suggested that propranolol is acting through its blockade of beta-mediated renin release and/or through its so-called membrane-stabilizing effect.

Acute Kidney Injury↗
PubMed1977

Feedback control of glomerular filtration rate in isolated, blood-perfused dog kidneys.

Micropuncture studies were done in isolated, blood-perfused dog kidneys to investigate the intrarenal nature of tubuloglomerular feedback regulation of nephron filtration rate. Collections were made at early proximal tubular sites during alterations in flow through the loop of Henle to elicit the feedback response. Renal blood flow in the 10 isolated kidneys averaged 4 ml/ min-g kidney after an initial vasoconstriction. Filtration rate was 0.52 +/- 0.12 ml/min-g kidney for the period 90-120 min, but progressively fell after 120 min, as did fractional sodium reabsorption and PAH extraction. The feedback regulation of nephron filtration rate was demonstrated during the first 3 hrs of perfusion even with subnormal renal function. The feedback response expressed as the percent reduction of early proximal flow rate when loop of Henle flow was elevated from 0 to 45 nl/min was 41.3 +/- 4.5 (for the first 90 min), 35.3 +/- 7.5 (90-120 min), 24.3 +/- 6.8 (120-150 min), and 26.6 +/- 7.7% (150-180 min). After 180 min, the feedback response was no longer demonstrated. These results show that feedback-induced changes in nephron filtration rate are achieved in the absence of nervous system influences.

Animals↗