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PubMed1988

Sympathetic activation induces asynchronous contraction in awake dogs with regional denervation.

To determine effects of regional left ventricular (LV) denervation on regional contractile responses to sympathetic activation, dogs with posterior LV wall denervation (posterior wall-denervated group) and dogs with innervated posterior LV walls (intact group) were studied during excitement, exercise, bilateral sympathetic nerve stimulation, and norepinephrine infusion. In intact conscious dogs, all modes of sympathetic activation increased the magnitude and decreased the time of onset of systolic wall thickening (WT) similarly in the anterior and posterior wall. In the denervated group, excitement failed to increase posterior WT during systole but instead elicited asynchronous contraction, i.e., postsystolic WT, as well as delayed onset of contraction. Asynchronous contraction was not observed with excitement after beta-adrenergic receptor blockade. Asynchronous contraction of the posterior wall was also observed during the initial phase of exercise in conscious dogs and during bilateral stellate stimulation in anesthetized dogs in the posterior wall-denervated group. In comparison to neural activation, adrenergic receptor activation with norepinephrine (0.2 microgram/kg-1.min-1 iv) induced a supersensitive increase in systolic WT in the denervated posterior wall (36 +/- 5%) compared with the anterior wall (17 +/- 2%) and a delay in the end of contraction in the anterior region. Thus asynchronous contraction can be elicited in dogs with regional LV denervation as a result of an early and enhanced contraction in the innervated region during neural sympathetic activation. The reverse was observed with systemic administration of norepinephrine because of catecholamine supersensitivity in the denervated posterior wall.

Animals↗
PubMed1986

Phospholipids, prostaglandin E2, and proteolysis in denervated muscle.

Soleus muscles of rats were studied up to 16 days after sciatic nerve transection. At the end of this period the denervated soleus muscles exhibited decreased content of diphosphatidylglycerol (-44%), normal level of phosphatidylethanolamine, and increased contents of phosphatidylcholine (+24%), sphingomyelin (+48%), lysophosphatidylcholine (+110%), phosphatidylinositol (+37%), and phosphatidylserine (+40%) per milligram of tissue protein. In studies in vitro, prostaglandin E2 (PGE2) release and tyrosine release by denervated soleus muscles were 319 and 141%, respectively, greater than those of sham muscles. An almost complete inhibition of PGE2 release with 5 X 10(-4) M aspirin or 2.8 X 10(-6) M indomethacin had no effect on tyrosine release of sham muscles or the stimulated tyrosine release of the denervated muscles. Addition of 5 X 10(-5) M cycloheximide in the medium resulted in 63% inhibition of PGE2 release by both groups of muscles; concomitant absolute increments in tyrosine releases by denervated and sham muscles did not statistically differ. In the presence of both 5 X 10(-5) M cycloheximide and 5 X 10(-4) M aspirin in the medium, PGE2 production by denervated and sham muscles was inhibited 87% while tyrosine release of denervated muscles was 108% higher than that of sham animals. It is concluded that 1) atrophy of denervated soleus muscle is associated with stimulated activity of tissue phospholipase A2, increased production of prostaglandin E2, increased total proteolytic rate, and unchanged rate of protein synthesis; 2) acute inhibition of PGE2 production does not inhibit the stimulated proteolysis in denervated muscle; and 3) cycloheximide inhibits PGE2 production by muscle.

Animals↗
PubMed1987

Dynamics of insulin resistance in denervated slow and fast muscles in vivo.

Sciatic nerve in one hindlimb of rats was sectioned, and animals were investigated 3, 6, 9, and 24 h and 3, 8, and 17 days after surgery. Cellular uptakes of 2-deoxy-D-glucose (DG) and alpha-aminoisobutyric acid (AIB) by soleus, plantaris, and gastrocnemius muscles of the denervated and contralateral sham hindlimb were compared in vivo. Effects of insulin on DG and AIB uptakes by soleus and plantaris muscles, but not gastrocnemius muscles, were reduced 20-58% as early as 3-6 h after denervation. Three to 17 days after denervation, soleus muscle did not respond to insulin stimulation of DG uptake, whereas plantaris and gastrocnemius muscles responded, but the insulin-induced increment in DG uptake was reduced 24-68% compared with the sham muscles. In contrast, none of the denervated muscles increased AIB uptake in response to insulin stimulation 3-17 days after surgery. The levels of creatine phosphate and ATP in calf muscles frozen in situ 3 days after denervation were increased 7 and 9%, respectively, and those of ADP, AMP, glucose-6-phosphate, and lactate were unchanged compared with sham muscles. It is concluded that muscle denervation results in a rapid development of insulin resistance, the effect of denervation depends on muscle fiber population, and insulin resistance of denervated muscles is not due to a cellular energy deficit.

Aminoisobutyric Acids↗
PubMed1988

Effects of denervation and immobilization on collagen synthesis in rat skeletal muscle and tendon.

The activities of prolyl 4-hydroxylase (PH) and galactosylhydroxylysyl glucosyltransferase (GGT), both enzymes of collagen biosynthesis, and the concentration of hydroxyproline (HYP) were measured in the gastrocnemius, soleus, and tibialis anterior muscles of rats after sciatic nerve neurectomy combined with cast immobilization of the denervated limb for 1 and 3 wk. PH and GGT were also observed in Achilles and tibialis anterior tendons after cast immobilization without neurectomy. After neurectomy the specific PH activity in the denervated gastrocnemius muscle increased by 215% (P less than 0.001). The specific GGT activity increased by 92-110% (P less than 0.01) in the denervated gastrocnemius, soleus, and tibialis anterior muscles. Elevation of the muscular HYP concentration by 118-170% (P less than 0.001) in the denervated muscles was observed. The PH, GGT, and HYP responses of the denervated muscles immobilized at a lengthened or shortened position during denervation atrophy did not generally differ significantly from those of the unfixed denervated ones. The specific PH and GGT activities of the disused tendons decreased by 62 (P less than 0.01) and 25% (P less than 0.001), respectively, in tendons immobilized in a chronically shortened position. The results suggest that denervation atrophy of skeletal muscle is associated with both an increased level of muscular collagen biosynthesis and with an increased muscular collagen concentration. The PH and GGT responses of the cast-immobilized tendons suggest adaptive changes in collagen biosynthesis of the disused tendon.

Adaptation, Physiological↗
PubMed1997

GLUT-4 protein and citrate synthase activity in distally or proximally denervated rat soleus muscle.

The potential role of neurotrophic factors in the decline of glucose transporter (GLUT-4) protein levels and citrate synthase (CS) activity was studied by comparing distally with proximally denervated juvenile rat soleus muscle. Severing of the tibial nerve produced distal (long stump) or proximal (short stump) denervation. GLUT-4 levels and CS activities were measured at 24-h intervals for up to 96 h after denervation. No differences were observed in GLUT-4 or CS activity between soleus muscles left with short or long nerve stumps at any time point. However, within just 24 h, denervation decreased (P < 0.05). GLUT-4 and CS (67.4 +/- 3.3 and 63.4 +/- 1.7% of innervated control values, respectively). Both parameters continued to decline up to 96 h (44.4 +/- 3.1 and 48.7 +/- 4.0%, respectively). There was a significant correlation between the GLUT-4 protein level and CS activity over this 96-h period of denervation (r = 0.653, P < 0.001). A similar response in the 24-h denervated soleus of adult rats was observed. In contrast, 24-h denervation of red gastrocnemius (type IIa fibers) left with a long nerve stump resulted in a prevention of the decline of GLUT-4 and CS seen in red gastrocnemius left with a short nerve stump in both juvenile and adult animals. These results suggest that unlike type IIa muscles, the decline in GLUT-4 level and CS activity in type I soleus muscle after denervation results from a lack of coordinated electrical activity but likely does not involve a neurotrophic agent. These results also support the hypothesis that there is coregulation of decreased expression of GLUT-4 protein and CS activity in this model of reduced neuromuscular activity.

Animals↗
PubMed2000

Regulation of myogenin protein expression in denervated muscles from young and old rats.

Myogenin is a muscle-specific transcription factor participating in denervation-induced increases in nicotinic ACh receptor (nAChR) gene expression. Although myogenin RNA expression in denervated muscle is well documented, surprisingly little is known about myogenin protein expression. Therefore, we assayed myogenin protein and RNA in innervated and denervated muscles from young (4 mo) and old (24-32 mo) rats and compared this expression to that of the nAChR alpha-subunit RNA. These assays revealed increased myogenin protein expression within 1 day of denervation, preceding detectable increases in nAChR RNA. By 3 days of denervation, myogenin and nAChR alpha-subunit RNA were increased 500- and 130-fold, respectively, whereas myogenin protein increased 14-fold. Interestingly, old rats (32 mo) had 6-fold higher myogenin protein and approximately 80-fold higher mRNA levels than young rats. However, after denervation, expression levels were similar for young and old animals. The increased myogenin expression during aging, which tends to localize to small fibers, likely reflects spontaneous denervation and/or regeneration. Our results show that increased myogenin protein in denervated muscles correlates with the upregulation of its mRNA.

Aging↗
PubMed2001

Splenic denervation worsens lipopolysaccharide-induced hypotension, hemoconcentration, and hypovolemia.

During lipopolysaccharide (LPS)-induced endotoxemia, increased intrasplenic fluid efflux contributes to a reduction in plasma volume. We hypothesized that splenic sympathetic nerve activity (SSNA), which increases during endotoxemia, limits intrasplenic fluid efflux. We reasoned that splenic denervation would exaggerate LPS-induced intrasplenic fluid efflux and worsen the hypotension, hemoconcentration, and hypovolemia. A nonlethal dose of LPS (150 microg x kg(-1) x h(-1) for 18 h) was infused into conscious male rats bearing transit time flow probes on the splenic artery and vein. Fluid efflux was estimated from the difference in splenic arterial inflow and venous outflow (A-V). LPS significantly increased the (A-V) flow differential (fluid efflux) in intact rats (saline -0.01 +/- 0.02 ml/min, n = 8 vs. LPS +0.21 +/- 0.06 ml/min, n = 8); this was exaggerated in splenic denervated rats (saline -0.03 +/- 0.01 ml/min, n = 7 vs. LPS +0.41 +/- 0.08 ml/min, n = 8). Splenic denervation also exacerbated the LPS-induced hypotension, hemoconcentration, and hypovolemia (peak fall in mean arterial pressure: denervated 19 +/- 3 mmHg, n = 10 vs. intact 12 +/- 1 mmHg, n = 8; peak rise in hematocrit: denervated 6.7 +/- 0.3%, n = 8 vs. intact 5.0 +/- 0.3%, n = 8; decrease in plasma volume at 90-min post-LPS infusion: denervated 1.08 +/- 0.15 ml/100 g body wt, n = 7 vs. intact 0.54 +/- 0.08 ml/100 g body wt, n = 8). The exaggerated LPS-induced hypovolemia associated with splenic denervation was mirrored in the rise in plasma renin activity (90 min post-LPS: denervated 11.5 +/- 0.8 ng x ml(-1) x h(-1), n = 9 vs. intact 6.6 +/- 0.7 ng x ml(-1) x h(-1), n = 8). These results are consistent with our proposal that SSNA normally limits LPS-induced intrasplenic fluid efflux.

Animals↗
PubMed1985

Renal prostanoids after unclipping the denervated one-kidney, one-clip hypertensive rat.

The contribution of the renal nerves in maintaining blood pressure and modulating renal prostanoid synthesis was examined in established (less than 8 wk in duration) one-kidney, one-clip (1K,1C) hypertension in the rat. Systolic blood pressure was measured for 7 days after renal denervation, at which time the renal artery clip was removed. Twenty-four-hour urinary excretion of PGE2 and 6-keto-PGF1 alpha (stable degradation product of PGI2) was determined before and after denervation and unclipping. Compared with sham-denervated rats, denervation (n = 15) resulted in a small but significant fall in blood pressure (from 216 +/- 4 to 182 +/- 4 mmHg after 48 h) and an increase in urinary 6-keto-PGF1 alpha (from 31 +/- 4 to 43 +/- 5 ng/24 h after 24 h). There was no change in PGE2 excretion. Seven days after surgery, blood pressures were similar in denervated (202 +/- 4 mmHg) and sham-denervated (211 +/- 5 mmHg) rats and fell to a similar extent 24 h after unclipping (142 +/- 3 and 147 +/- 4 mmHg, respectively). Urinary 6-keto-PGF1 alpha increased from 25 +/- 5 to 74 +/- 11 in denervated and 21 +/- 2 to 72 +/- 9 ng/24 h in sham-denervated rats in the 24 h after unclipping. PGE2 excretion increased approximately twofold over this period. These findings indicate that the renal nerves have only a minor role in established hypertension in the 1K,1C rat and that the reversal of hypertension and stimulation of renal prostanoid synthesis following unclipping is not dependent on neural mechanisms.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

Regulation of glucose transporters GLUT-4 and GLUT-1 gene transcription in denervated skeletal muscle.

Because GLUT-4 expression is decreased whereas GLUT-1 expression is increased in denervated skeletal muscle, we examined the effects of denervation on GLUT-4 and GLUT-1 gene transcription. The right hindlimb skeletal muscle of male transgenic mice containing sequential truncations (2,400, 1,639, 1,154, and 730 bp) of the human GLUT-4 promoter linked to the chloramphenacol acyl transferase (CAT) gene was denervated, and the contralateral hindlimb was sham operated. RNase protection analysis revealed that after 72 h denervation decreased CAT mRNA and GLUT-4 mRNA levels 64-85%, respectively (P < 0.05), in the gastrocnemius muscles. In contrast, denervation of the right hindlimb of male rats increased GLUT-1 gene transcription and GLUT-1 mRNA levels by 94 and 213%, respectively (P < 0.05). In conclusion, GLUT-4 transcription is decreased but GLUT-1 transcription is increased in denervated skeletal muscle, suggesting that the effects of denervation on GLUT-4 and GLUT-1 expression are, in part, transcriptionally mediated. Furthermore, these data indicate that a DNA sequence regulated by denervation is located within 730 bp of the 5'-flanking promoter region of the human GLUT-4 gene.

Animals↗
PubMed2001

Lipoprotein lipase activity in skeletal muscles of the rat: effects of denervation and tenotomy.

The effects of denervation, tenotomy, or tenotomy with simultaneous denervation on the activity of heparin-releasable and intracellular, residual lipoprotein lipase (LPL) and triacylglycerol (TG) content were examined in rat skeletal muscles. An influence of muscle electrostimulation on denervated and tenotomized muscles was also evaluated. Activity of both LPL fractions was decreased in denervated and/or tenotomized soleus and red portion of gastrocnemius muscles. It was accompanied by a slight elevation of the intracellular TG content. Electrostimulation increased activities of both fractions of LPL in red muscles from intact hindlimbs. In stimulated denervated muscles without or with simultaneous tenotomy, activity of two LPL fractions was also enhanced, but control values were reached only in denervated soleus muscle. Electrical stimulation had no pronounced effect on LPL activity in tenotomized muscles. In conclusion, denervation and/or tenotomy decreases LPL activity in red muscles, indicating reduction of the muscle potential to utilize circulating TG. Electrostimulation only partly restores the diminished LPL activity in denervated muscles, without any effect in tenotomized ones. Thus, to maintain LPL activity in resting muscle, intact innervation and tension are needed.

Achilles Tendon↗
PubMed2001

AMP-activated protein kinase activation prevents denervation-induced decline in gastrocnemius GLUT-4.

This study was designed to determine whether the reductions in GLUT-4 seen in 3-day-denervated muscles can be prevented through chemical activation of 5'-AMP-activated protein kinase (AMPK). Muscle AMPK can be chemically activated in rats using subcutaneous injections with 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR). In this study, the tibial nerve was sectioned on one side; the other was sham operated but without nerve section. Acute injections of AICAR resulted in significantly increased AMPK activity in denervated gastrocnemius but not soleus muscles. Acetyl-CoA carboxylase activity, a reporter of AMPK activation, declined in both gastrocnemius and soleus in both denervated and contralateral muscles. Three days after denervation, GLUT-4 levels were significantly decreased by approximately 40% in gastrocnemius muscles and by approximately 30% in soleus muscles. When rats were injected with AICAR (1 mg/g body wt) for 3 days, the decline in GLUT-4 levels was prevented in denervated gastrocnemius muscles but not in denervated soleus muscles. The extent of denervation-induced muscle atrophy was similar in AICAR-treated vs. saline-treated rats. These studies provide evidence that some effects of denervation may be prevented by chemical activation of the appropriate signaling pathways.

AMP-Activated Protein Kinases↗
PubMed1992

Proportional enlargement of motor units after partial denervation of cat triceps surae muscles.

1. To determine the capacity of motoneurons to increase their motor unit (MU) size by collateral sprouting and to assess this capacity in relation to the size of the motor nerve, we partially denervated soleus, lateral gastrocnemius (LG), and medial gastrocnemius (MG) muscles in adult and neonatal cats. Isometric force and extracellular nerve potentials were recorded from > or = 7% of the remaining MUs, 2.5-18 mo later. S1 or L7 roots were sectioned unilaterally and the number of remaining MUs was quantified by use of charge and force measurements. 2. The mean unit force increased inversely with MU number in partially denervated muscles, but the increase was less than predicted for extensive denervations (> or = 90%). The same enlargement of MU size occurred whether muscles were partially denervated in neonatal or adult animals. 3. The force distribution of MUs in partially denervated muscles was similar to normal but was shifted to larger force values in direct proportion to the extent of partial denervation (PD). All MUs increased in size by the same factor to preserve the normal force distribution. 4. Normal size relationships among force, contractile speed, and axon potential amplitude were observed for MUs in partially denervated muscles. Because changes in muscle fiber size could not account for the increase in unit force, these data show that increase in MU size, with respect to unit force and innervation ratio (muscle fibers per motoneuron), is proportional to the size of the motor nerve. 5. Enlargement of MU size in partially denervated muscles did not have a retrograde effect on nerve fiber caliber because axon potential amplitude and conduction velocity were not changed after PD. 6. Under conditions of extensive PD (> 85%), regenerated nerves from the cut spinal root reinnervated the gastrocnemius muscles. It is likely that nerves supplied muscle fibers that were not innervated by sprouts from nerves in the uncut root as well as displacing sprouts from terminals in extensively enlarged MUs. 7. We conclude that all motoneurons within a motor pool compensate for partial nerve injuries by collateral sprouting and that enlargement of MU size is a function of motor nerve size, consistent with Henneman's size principle.

Action Potentials↗
PubMed1975

Effects of renal nerves on renal hemodynamics. II. Renal denervation models.

The effect of acute renal denervation on renal blood flow (RBF) and intrarenal distribution of blood flow (microsphere method) was studied in dogs using three standard denervation models. Surgical denervation, by stripping renal vascular nerves and autoperfusing the kidney through a large bore plastic catheter, caused RBF and glomerular filtration rate to decrease. Also, intrarenal distribution of blood flow became asymmetric, that is, perfusion changes in the two halves of the kidney were not similar. Denervation by stripping away the neural tissue and infiltrating the hilum with 0.5% procaine and 50% ethanol produced no adverse effects on RBF, but distributional changes were asymmetric. Denervation by this method was probably incomplete as evidenced by decreased RBF following bilateral carotid occlusion. Intrarenal arterial infusion of 10 mug/kg/min phenoxybenzamine caused renal perfusion to change asymmetrically and did not abolish the decrease in RBF normally seen following nerve stimulation. Present results demonstrate denervation studies must be interpreted cautiously; because the denervation model may cause renal damage and asymmetric perfusion, and denervation may not be complete.

Animals↗
PubMed2002

Effect of arterial baroreceptor denervation on sodium balance.

During chronic increased dietary sodium intake, arterial baroreceptors buffer against sustained increases in arterial pressure, and renal sympathoinhibition contributes importantly to the maintenance of sodium balance by decreasing renal tubular sodium reabsorption and increasing urinary sodium excretion. The present study examined the effect of arterial baroreceptor denervation on sodium balance in conscious rats during low, normal, and high dietary sodium intake. Compared with measurements made before arterial baroreceptor denervation, arterial baroreceptor-denervated rats had similar sodium balance during normal dietary sodium intake but significantly more negative sodium balance during low dietary sodium intake and significantly more positive sodium balance during high dietary sodium intake. At the end of the high dietary sodium intake period, arterial pressure (under anesthesia) was 159+/-5 mm Hg after arterial baroreceptor denervation and 115+/-1 mm Hg before arterial baroreceptor denervation. Sham arterial baroreceptor denervation in time control rats had no effect on sodium balance or arterial pressure during the different dietary sodium intakes. These studies indicate that (1) arterial baroreceptor denervation impairs the ability to establish sodium balance during both low and high dietary sodium intake, and (2) arterial baroreceptor denervation leads to the development of increased arterial pressure during high dietary sodium intake in association with increased renal sodium retention.

Animals↗
PubMed1989

Protection against autonomic denervation following acute myocardial infarction by preconditioning ischemia.

To examine the effects of ischemic preconditioning on efferent autonomic responses following acute transmural myocardial ischemia/infarction (MI), the time course and extent of efferent sympathetic and vagal denervation were compared between control dogs that received a one-stage sustained coronary occlusion and preconditioned dogs that received four 5-minute coronary occlusions separated by 5 minutes of reperfusion before sustained occlusion. Effective refractory periods (ERP) basal and apical to MI were determined in the baseline state and during neural stimulation before and after preconditioning occlusions and 20, 60, 120, and 180 minutes after sustained occlusion by ligature ligation of diagonal branches of the left anterior descending coronary artery. In 10 control dogs with transmural MI, ERP shortening induced by bilateral ansae subclaviae stimulation (4-msec pulses, 2-4 Hz and 2-4 mA) was unchanged at basal sites but was attenuated at apical sites. Four of 40 apical test sites exhibited efferent sympathetic denervation (less than or equal to 2 msec shortening) 20 minutes after sustained occlusion. Thirteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, ERP shortening at apical sites was unchanged after preconditioning occlusions and during the first 60 minutes of sustained ischemia but was attenuated at 120 minutes. Three of 40 apical test sites became denervated during a 3-hour period. The cumulative percentage of denervated apical test sites was significantly less in the preconditioned group compared with the control group (p = 0.006) despite a comparable degree of subepicardial involvement in the MI (8.2 +/- 1.0% vs. 8.4 +/- 1.4%, the ratio to the left ventricular circumference, mean +/- SEM). In 11 control dogs tested for efferent vagal response after MI, ERP prolongation induced by bilateral vagal stimulation (4-msec pulses, 20 Hz with current strength 0.05 mA greater than that required to produce asystole) was unchanged at basal sites, but was attenuated at apical sites, and five of 44 test sites exhibited denervation (less than or equal to 1 msec prolongation) 20 minutes after sustained coronary occlusion. Fourteen of 40 apical sites became denervated during a 3-hour period. In 10 preconditioned dogs, vagally induced ERP prolongation was unchanged both at basal and apical sites, and none of 36 apical test sites exhibited denervation after preconditioning and during a 3-hour period of sustained coronary occlusion (p less than 0.001 vs. control group) despite a comparable degree of subendocardial involvement in the MI (11.8 +/- 0.8% vs. 11.9 +/- 1.3%).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1997

Increased type I procollagen mRNA in airways and pulmonary vessels after vagal denervation in rats.

To test the hypothesis that increased airway strain resulting from lung denervation initiates a fibroproliferative response in the airways, we compared the transcriptional expressions of alpha1(I)-procollagen and tropoelastin in the lungs of rats subjected to unilateral vagal denervation, unilateral vagal denervation combined with ipsilateral phrenectomy, or thoracotomy without denervation (controls). We found increases in alpha1(I)-procollagen messenger ribonucleic acids (mRNAs) in the submucosa of the airways and the adventitia of airways and pulmonary vessels of the denervated lungs in 31% of the rats subjected to unilateral denervation (with and without phrenectomy), and in none of the controls. The increased transcripts were associated with collagen deposition in the peribronchial and perivascular tissue, and occasionally with cell proliferation leading to occlusion of the airway and vascular lumina. Unilateral phrenectomy did not decrease the frequency with which production of Type I procollagen was upregulated, suggesting that the upregulation was not entirely dependent on airway strain. Tropoelastin expression was not influenced by denervation. Our results indicate that the autonomic nervous system has a previously unsuspected trophic influence on collagen synthesis in the airways and pulmonary vessels. Abolition of this influence by denervation may lead to structural changes analogous to those observed in bronchiolitis obliterans after lung transplantation.

Animals↗
PubMed1986

Changes in glomerular hemodynamic response to angiotensin II after subacute renal denervation in rats.

We examined the changes in glomerular hemodynamics produced by angiotensin II (AII) in both normal Munich-Wistar rats and rats which were unilaterally renal denervated (measured kidney) 4-6 d prior to the measurement periods. Measurements of glomerular dynamics were performed in a control period after plasma volume expansion and during infusion of 11 ng X 100 g body wt-1 X min-1 of AII. The glomerular hydrostatic pressure gradient increased from 38 +/- 1 to 49 +/- 1 mmHg in denervated rats compared with a lesser response in controls (from 39 +/- 1 to 45 +/- 1 mmHg, P less than 0.05). Single nephron plasma flow decreased from 213 +/- 17 to 87 +/- 4 nl X min-1 X g kidney wt (KW)-1 in denervated kidneys versus a more modest decrease in control kidneys (from 161 +/- 9 to 102 +/- 5 nl X min X gKW-1). These changes were due to a greater increase in both afferent and efferent arteriolar resistance after AII infusion in denervated compared with control kidneys. Glomerular AII receptor maximum binding was 1,196 +/- 267 fmol/mg protein in denervated kidneys compared with 612 +/- 89 fmol/mg protein (P less than 0.01) in controls with no change in receptor affinity. We conclude the subacute unilateral renal denervation results in renal vasodilation, denervation magnifies the vasoconstrictive effect of AII infusion on glomerular hemodynamics, and the observed increased response to AII after denervation is associated with increases in glomerular AII receptors.

Angiotensin II↗
PubMed1993

Local sympathetic denervation of white adipose tissue in rats induces preadipocyte proliferation without noticeable changes in metabolism.

The direct influence of the sympathetic nervous system on white adipose tissue was studied by performing a unilateral surgical denervation of the retroperitoneal fat pad in rats, the contralateral pad being used as a control. One week after surgery, the weight of the denervated pad was significantly higher than that of the intact pad. In vivo, glucose utilization was not altered by denervation. The expression of GLUT4 as well as the expression and activity of fatty acid synthase, lipoprotein lipase, and hormone-sensitive triglyceride lipase were similar in the two pads. Lipolysis in response to norepinephrine, determined in vitro, was not modified by denervation although the ratio between alpha 2- and beta-adrenergic receptors was changed. Denervation induced an increase in DNA content without change in the number of mature adipocytes. The expression of A2COL6/pOb24, a marker of the early step of adipocyte differentiation, was significantly enhanced in the denervated pad, suggesting an increased number of preadipocytes. This was confirmed by an increased cell number observed in the denervated fat pad 1 month after surgery. In conclusion, surgical denervation of the white fat pad does not alter the glucose and lipid metabolisms. By contrast, it accelerated adipocyte differentiation and led to the recruitment of new precursors.

Adipose Tissue↗