Renal Dopamine Receptor Signaling Mechanisms in Spontaneously Hypertensive and Fischer 344 Old Rats

The inability of old rats to maintain body temperature during cold exposure has been well documented. This study evaluated the effect of exercise on the rates of cold-induced O2 consumption and the contribution of nonshivering thermogenesis (NST) to these rates. Younger (12 mo) and older (24 mo) male Fischer 344 (F344) rats were divided into exercised and sedentary groups. Exercised rats were run on a motor-driven treadmill 60 min/day, at 19-24 m/min, 5 days/wk for 6 mo. At the conclusion of the 6-mo training period, O2 consumption of all four groups was measured at thermoneutrality (26 degrees C) and during 6 h of exposure to 6 degrees C. Rectal temperatures were recorded before and after cold exposure. NST was estimated from the ability of isolated brown fat mitochondria to bind guanosine 5'-diphosphate (GDP). Core temperature of older sedentary rats fell 5.1 +/- 0.4 degrees C after cold exposure (36.3 +/- 0.3 vs. 31.2 +/- 0.8 degrees C). Exercise training in older animals prevented this fall from occurring (36.4 +/- 0.2 vs. 35.3 +/- 0.3 degrees C). Core temperatures of cold-exposed younger exercised and sedentary rats did not differ from thermoneutral values. Exercise did not alter the rates of resting body mass-independent (ml.min-1.kg body mass-0.67) O2 consumption in younger or older rats. However, body mass-independent and lean body mass (LBM)-independent (ml.min-1.g LBM-0.67) cold-induced O2 consumptions of older exercised rats were significantly elevated relative to those of older sedentary animals. This effect of exercise was not seen in younger rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Download Full-text

Cross-talk between an activator of nuclear receptors-mediated transcription and the D1 dopamine receptor signaling pathway

Pharmacology Biochemistry and Behavior ◽

10.1016/j.pbb.2004.11.013 ◽

2005 ◽

Vol 80 (3) ◽

pp. 379-385 ◽

Cited By ~ 3

Author(s):

Azriel Schmidt ◽

Robert Vogel ◽

Su Jane Rutledge ◽

Evan E. Opas ◽

Gideon A. Rodan ◽

...

Keyword(s):

Signaling Pathway ◽

Dopamine Receptor ◽

Nuclear Receptors ◽

Cross Talk ◽

Receptor Signaling ◽

D1 Dopamine Receptor ◽

Receptor Signaling Pathway

Download Full-text

Overexpression of PKC-βI and -δ contributes to higher PKC activity in the proximal tubules of old Fischer 344 rats

AJP Renal Physiology ◽

10.1152/ajprenal.00198.2003 ◽

2003 ◽

Vol 285 (6) ◽

pp. F1100-F1107 ◽

Cited By ~ 15

Author(s):

Mohammad Asghar ◽

Tahir Hussain ◽

Mustafa F. Lokhandwala

Keyword(s):

Skf 38393 ◽

Proximal Tubules ◽

Fischer 344 Rats ◽

Adult Rats ◽

Altered Expression ◽

Fischer 344 ◽

Pkc Isoforms ◽

Diuretic Response ◽

Old Rats ◽

Pkc Ζ

Previously, we reported that natriuretic and diuretic response to dopamine is diminished in old Fischer 344 rats, which is due to higher basal protein kinase C (PKC) activity and hyperphosphorylation of Na-K-ATPase in the proximal tubules (PTs) of old rats. The present study was conducted to determine whether higher PKC activity could be due to altered expression of some of the PKC isoforms in the superficial cortex (rich in PTs) of old rats. Fluorimetric measurement showed almost twofold increase in the PKC activities in homogenates and membranes of old (24 mo) compared with adult (6 mo) rats. Interestingly, in the basal state PKC-βI was overexpressed in the membranes, whereas PKC-δ expression was increased in the cytosol of old compared with adult rats. Treatment of the cortical slices with either SKF-38393, a D1-like agonist, or PDBu, a direct activator of PKC, caused translocation of PKC-βI from cytosol to membranes in adult but not in old rats. Both of these drugs caused translocation of PKC-δ from membranes to cytosol in adult but not in old rats. These drugs had no effect on translocation of PKC-ζ in both adult and old rats. Both PKC-βI and -δ coimmunoprecipiated with α1-subunit of Na-K-ATPase in adult and old rats. These observations suggest that both SKF-38393 and PDBu differentially regulate PKC-βI and -δ in adult but not in old rats. Also, PKC-βI and -δ seem to interact with Na-K-ATPase in these animals. The overexpression of both PKC-βI and -δ in old rats could be responsible for a higher basal PKC activity, which causes the hyperphosphorylation of Na-K-ATPase and contributes to the diminished inhibition of Na-K-ATPase activity by dopamine in old rats.

Download Full-text

Aging induces muscle-specific impairment of endothelium-dependent dilation in skeletal muscle feed arteries

Journal of Applied Physiology ◽

10.1152/japplphysiol.00461.2002 ◽

2002 ◽

Vol 93 (5) ◽

pp. 1685-1690 ◽

Cited By ~ 79

Author(s):

Christopher R. Woodman ◽

Elmer M. Price ◽

M. Harold Laughlin

Keyword(s):

Skeletal Muscle ◽

Mrna Expression ◽

Vascular Function ◽

Fischer 344 ◽

Old Rats ◽

The Right ◽

Oxide Synthase ◽

Endothelial Nitric Oxide ◽

Feed Arteries ◽

Skeletal Muscle Feed Arteries

We tested the hypothesis that aging decreases endothelium-dependent vasodilation in feed arteries perfusing rat skeletal muscle. In addition, we tested the hypothesis that attenuated vasodilator responses are associated with decreased endothelial nitric oxide synthase (eNOS) and superoxide dismutase-1 (SOD-1) expression. Soleus feed arteries (SFA) and gastrocnemius feed arteries (GFA) were isolated from young (4 mo) and old (24 mo) male Fischer 344 rats. Feed arteries from the right hindlimb were cannulated with two glass micropipettes for examination of endothelium-dependent [acetylcholine (ACh)] and endothelium-independent [adenosine (Ado) or sodium nitroprusside (SNP)] vasodilator function. Feed arteries from the left hindlimb were frozen and used to assess eNOS and SOD-1 protein and mRNA expression. In SFA, endothelium-dependent dilation to ACh was reduced in old rats (0.9 ± 0.04 vs. 0.8 ± 0.03), whereas dilator responses to Ado and SNP were similar in SFA of young and old rats. In GFA, vasodilator responses to ACh, Ado, and SNP were not altered by age. eNOS and SOD-1 protein expression declined with age in SFA (−71 and −54%, respectively) but not in GFA. eNOS and SOD-1 mRNA expression were not altered by age in SFA or GFA. Collectively, these data indicate aging induces muscle-specific impairment of endothelium-dependent vascular function in SFA.

Download Full-text