Biomedical subjects

D W Good

Publications and source records attributed to D W Good.

5 recordsLinked to original sources

PubMed1992

Effects of adenosine on ion transport in rat medullary thick ascending limb.

Previously, we demonstrated that adenosine (Ado) was released by the medullary thick ascending limb (MTAL) during hypoxia. The present experiments were designed to examine the effects of Ado and adenosine analogues on net chloride (JCl) and bicarbonate (JHCO3) absorption by the isolated, perfused MTAL of the rat. Ado, 10 nM, in the presence or absence of arginine vasopressin (AVP, 10(-10) M) reduced JCl by 50%. The inhibition of Ado was reproduced with the selective A1 agonist, N-6-phenylisopropyladenine (2 nM), and was reversed by 8-cyclopentyl-1,3-dipropylxanthine, an A1-receptor antagonist. Thus the inhibition of JCl is likely mediated through A1 receptors. In contrast, Ado had no effect on (JHCO3) either in the presence or absence of AVP. Ado also had no influence on the effect of AVP to inhibit JHCO3. The lack of effect on JHCO3 suggests that the inhibition of JCl by Ado is unlikely to be mediated through changes in cellular adenosine 3',5'-cyclic monophosphate. These results support the hypothesis that Ado released into the renal medulla during hypoxia may protect the MTAL from ischemic injury by directly inhibiting NaCl absorption and reducing transport-related oxygen consumption.

Absorption↗

PubMed1992

Chronic hyperkalemia impairs ammonium transport and accumulation in the inner medulla of the rat.

Previously we demonstrated in rats that chronic hyperkalemia had no effect on ammonium secretion by the proximal tubule in vivo but that high K+ concentrations inhibited ammonium absorption by the medullary thick ascending limb in vitro. These observations suggested that chronic hyperkalemia may reduce urinary ammonium excretion through effects on medullary transport events. To examine directly the effects of chronic hyperkalemia on medullary ammonium accumulation and collecting duct ammonium secretion, micropuncture experiments were performed in the inner medulla of Munich-Wistar rats pair fed a control or high-K+ diet for 7-13 d. In situ pH and total ammonia concentrations were measured to calculate NH3 concentrations for base and tip collecting duct and vasa recta. Chronic K+ loading was associated with significant systemic metabolic acidosis and a 40% decrease in urinary ammonium excretion. In control rats, 15% of excreted ammonium was secreted between base and tip collecting duct sites. In contrast, no net transport of ammonium was detected along the collecting duct in high-K+ rats. The decrease in collecting duct ammonium secretion in hyperkalemia was associated with a decrease in the NH3 concentration difference between vasa recta and collecting duct. The fall in the NH3 concentration difference across the collecting duct in high-K+ rats was due entirely to a decrease in [NH3] in the medullary interstitial fluid, with no change in [NH3] in the collecting duct. These results indicate that impaired accumulation of ammonium in the medullary interstitium, secondary to inhibition of ammonium absorption in the medullary thick ascending limb, may play an important role in reducing collecting duct ammonium secretion and urinary ammonium excretion during chronic hyperkalemia.

Ammonia↗

PubMed1991

Effects of graded oxygen tension on adenosine release by renal medullary and thick ascending limb suspensions.

Adenosine is released from renal cells, and extracellular adenosine may influence the effects of ischemia on medullary tubule segments by altering ion transport or renal hemodynamics. While adenosine release and excretion are enhanced during renal ischemia, the specific sites of renal adenosine production have not been completely elucidated. In the present study, extracellular adenosine concentrations in suspensions of renal outer medulla and thick ascending limb segments were quantitated by reversed-phase high performance liquid chromatography. Media from other medullary (OM) suspensions incubated for 8 and 15 minutes at 0% oxygen contained significantly greater amounts of adenosine (1.404 +/- 0.21 and 2.034 +/- 0.27 ng/micrograms protein, respectively), when compared to values obtained from media of suspensions incubated for equivalent periods under non-hypoxic conditions (8, 20, and 95% oxygen), 0.78 +/- 0.05 (8 min) and 1.37 +/- 0.21 ng/micrograms protein (15 min). Similarly, adenosine release was greater in medullary thick ascending limb (mTAL) suspensions incubated for 8 minutes at 0% versus 8% oxygen (0.81 +/- 0.17 vs. 0.20 +/- 0.12 ng/micrograms protein, respectively). Moreover, the observed increase in adenosine release by thick ascending limbs at 0% oxygen could be inhibited completely by either furosemide or ouabain. These studies demonstrate that: 1) the renal medulla and medullary thick ascending limb are sites of adenosine release; 2) adenosine release by the mTAL is enhanced significantly during hypoxic conditions; and 3) the increased release of adenosine during hypoxia appears to be related to ion transport and oxidative metabolism, as the increased release was prevented by two disparate inhibitors of transport in this segment.

Adenosine↗

PubMed1979

Luminal influences on potassium secretion: sodium concentration and fluid flow rate.

Two methods of in vivo continuous microperfusion were used to evaluate separately luminal sodium concentration and fluid flow rate as factors regulating potassium secretion by the renal distal tubule of the rat. Emphasis was placed on evaluating changes in sodium concentration (43-97 mM) and flow rate (4-27 nl/min) within the physiological range. Absolute rates of Na, K, Cl, and H2O transport were measured. Results showed that increasing early distal flow rate without increasing early distal Na concentration significantly increased the absolute rate of potassium secretion by the distal tubule. In contrast, increasing early distal Na concentration, distal Na delivery, and distal Na absorption did not affect potassium secretion if flow rate was not changed. Further studies showed that reducing early distal Na concentration below the physiological range (to 15 mM) caused the direction of net sodium transport to be reversed but did not significantly reduce potassium secretion. Increasing early distal K concentration (to 34 mM) caused the direction of net potassium transport to be reversed. The rate of potassium secretion appears to depend in part on the luminal potassium concentration. Increases in luminal flow rate may increase the rate of potassium secretion by lowering the luminal K concentration.

Animals↗

PubMed1976

Group home program.

The success in this program was defined in terms of staying out of the hospital or in not regressing to a more intensive level of care requirement. By these criteria, we have been successful. Nine chronic patients have lived in the group home. Of these nine, two have become totally independent, five live in the group home, one went to a family care home, and one to a nursing home due to physical disease. Not one of the group is in a psychiatric institution, and only one had a setback. Presently, plans to expand this program with the assistance of a community group are being formulated.

Chronic Disease↗