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PubMed1981

Cerebrovascular response to hypoxia in baroreceptor- and chemoreceptor-denervated dogs.

Cerebral hemodynamic responses to arterial hypoxemia were studied in anesthetized paralyzed dogs that were or that had undergone carotid baroreceptor denervation, carotid chemoreceptor denervation, vagotomy, or both vagotomy and carotid sinus nerve section. Arterial O2 content was lowered from control (19.0 vol%) to 9.6 vol% by either decreasing arterial O2 tension [hypoxic hypoxemia (HH)] or increasing carboxyhemoglobin saturation[carbon-monoxide hypoxemia (COH)] at normal O2 tension. In intact animals (composite control values from all groups) HH and COH resulted in similar increases in cerebral blood flow (to 205 and 197% of control, respectively). Cerebral vascular resistance decreased more with COH than with HH (to 42 vs. 60% of control). The response from carotid baroreceptor-denervated animals and from vagotomized animals did not differ from that of the intact animals. After carotid chemoreceptor denervation and combined carotid sinus nerve section and vagotomy, both HH and COH increased cerebral blood flow to 194% of control (same increase as in intact animals, carotid baroreceptor-denervated animals, and vagotomized animals) and produced equal reductions in cerebral vascular resistance (to 34% of control). These data show that the carotid and aortic chemoreceptors are not necessary for the increase in cerebral blood flow provoked by hypoxemia and that this response is not modified by the carotid and aortic baroreceptors.

Animals↗
PubMed1982

Effects of left atrial stretch in cardiac-denervated and intact conscious dogs.

We monitored cardiovascular and renal function in conscious dogs with surgically denervated hearts during two experimental procedures: 1) inflation of a balloon in the left atrium and 2) intravascular volume expansion. The results obtained were compared with results from identical experiments on sham-operated control dogs. Left atrial balloon inflation in the sham-operated dogs produced an increase in left atrial pressure, heart rate, urine flow, and sodium excretion; central venous pressure decreased. These changes were absent in the cardiac-denervated dogs. Infusion of 6% dextran in isotonic saline (16% of estimated blood volume) increased the heart rate significantly in the control dogs but not in the cardiac-denervated dogs; other hemodynamic measurements were comparable in the two groups. Urine flow and sodium excretion increased significantly in both the cardiac-denervated and control dogs; the responses did not differ significantly between the two groups. These experiments demonstrate that inflation of a balloon in the left atrium of a conscious dog elicits diuretic and natriuretic responses that are dependent on intact cardiac neural pathways, presumably specifically dependent on afferent neural impulses from left atrial receptors. On the other hand, an increase in circulating blood volume induced by the intravenous infusion of an isotonic, isoncotic solution elicits diuretic and natriuretic responses in the cardiac-denervated dog that are similar to the renal responses produced in a control dog. Thus, although cardiac receptors are capable of eliciting reflex changes in both hemodynamics and renal function, it is not clear what role they play in mediating the renal responses evoked by increases in blood volume.

Animals↗
PubMed1983

Selective denervation of the heart.

Total denervation of the canine heart consisted of intrapericardial neural dissection of the left atrium, left superior pulmonary vein, and main pulmonary artery and cutting of the ventrolateral cardiac nerve (stage I). The fat pad and all nerves were removed from between the pulmonary artery and aorta (stage II). Dissection proceeded from the pericardial reflection along the superior vena cava to the azygos vein, which was cleared, double tied, and cut. The right pulmonary artery was cleaned, and the superior right atrium was dissected to its intersection with the left atrium (stage III). Denervation was tested by electrical stimulation of both vagi and stellate ganglia, while recording inotropic, chronotropic, and dromotropic events, before and after each stage. Stage I deleted most left autonomic input to the heart without interrupting right sympathetics. Stage II completed left autonomic denervation but preserved much of the right sympathetic input. Large nerves along the dorsal surface of the pulmonary artery carried inputs from both left and right sympathetics. Stage III completed the denervation of atrioventricular and sinoatrial nodal structures and removed all remaining ventricular inotropic influences. Selective denervation of atrioventricular and sinoatrial nodal regions appears feasible for preparation of chronic canine models.

Animals↗
PubMed1983

Altered nicotinic sensitivity of AV node in surgically denervated canine hearts.

The responses of normal and cardiac-denervated (DNV) dogs to acetylcholine (ACh) and nicotine (NIC) were examined to determine if the intrinsic cardiac nerves (ICN) that modulate electrical conduction display denervation supersensitivity. Control (n = 18) and DNV (n = 18) animals were placed on cardiopulmonary bypass. Recording of intra-atrial (P-A), intraventricular (H-V), and atrioventricular (AV) nodal (A-H) conduction times were made from the region of the His bundle. ACh (0.1-10 micrograms) was used to produce muscarinic stimulation, whereas NIC (0.1-400 micrograms) was employed to stimulate the ICN. All drugs were administered intracoronary. No supersensitivity to either ACh or NIC was seen in the data from the P-A or H-V intervals of the His electrogram in the DNV animals. However, this group displayed approximately a 10-fold increase in the negative dromotropic effect of NIC on the AV node compared with control. No significant change in muscarinic sensitivity of the AV node was observed in the DNV animals. We conclude that 1) no denervation supersensitivity of the ICN mediating effects on intra-atrial and intraventricular conduction occurs; 2) the AV node itself does not show muscarinic supersensitivity following extrinsic denervation; 3) the ICN do display denervation supersensitivity as shown by a 10-fold increase in the effects of NIC on AV nodal conduction time.

Acetylcholine↗
PubMed1995

Complexity and "chaos" in blood pressure after baroreceptor denervation of conscious dogs.

To investigate how arterial baroreceptors affect the dynamic properties of short-term blood pressure control, we determined Lyapunov exponents and correlation dimensions of blood pressure. Two groups of conscious dogs were studied: a control group (n = 7) and a group subjected to total sinoaortic and cardiopulmonary baroreceptor denervation (n = 7). As a measure of variability, standard deviation was determined and power spectra were calculated. In the lower frequency range (f < 0.1 Hz) power density was inversely related to frequency in both groups, indicating "1/f noise." Estimating the correlation dimension via the Grassberger-Procaccia algorithm as a quantification of complexity revealed a decrease after baroreceptor denervation (1.74 +/- 0.2 vs. 3.05 +/- 0.23 control; P < 0.05). Determination of the largest Lyapunov exponents lambda 1, which indicates the sensitive dependence on initial conditions, a hallmark of chaos, also yielded a diminution after denervation (lambda 1 = 0.74 +/- 0.08 vs. 1.85 +/- 0.18, P < 0.01). The results were cross-checked with surrogate data statistics. The null hypothesis, that there is no nonlinear structure in arterial blood pressure time series, was rejected. This shows that after baroreceptor denervation, blood pressure control is less complex and less sensitive to initial conditions ("chaos"). In contrast, variability (standard deviation) is increased (22.2 +/- 3.1 denervation vs. 8.3 +/- 1.4 control; P < 0.05). It is concluded that under physiological conditions, arterial and cardiopulmonary baroreceptors reduce variability of blood pressure, however, at the cost of blood pressure being less predictable. Thus the regulation is more sensitive depending on initial conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗
PubMed1980

Effect of liver denervation on the feeding pattern of rats.

This study was undertaken to assess the role of the hepatic innervation in the short-term regulatory mechanisms of food intake. A liver denervation was performed in male Wistar rats: the liver was entirely freed from the surrounding organs, its vessels (with the exception of the hepatic veins) and the bile ducts were stripped. Controls consisted of two groups of liver-denervated rats in which sympathectomy or vagotomy were carried out. A continuous recording of food intake was performed in a third group. The complete absence of the hyperglycemic response to trauma in adrenalectomized liver-denervated animals was taken as evidence of functional sympathectomy of the liver. The disappearance of a vagovagal reflex--heart rate variation brought about by a glucose injection into the portal vein--was taken as evidence of functional vagotomy. The analysis of the recorded feeding patterns of liver-denervated and sham-operated animals showed that, in rats, this liver denervation did not affect in any way the feeding behavior.

Afferent Pathways↗
PubMed1987

Augmented pressor response to vasopressin in awake dogs after cardiac denervation.

Hemodynamic responses to varying intravenous infusion rates of vasopressin were studied in two groups of dogs; one group was cardiac denervated and the other sham operated. Vasopressin given at 200, 1,000, and 5,000 fmol X kg-1 X min-1 produced increases in aortic pressure that were significantly greater in cardiac-denervated dogs than in sham-operated dogs. The augmented pressor response in cardiac-denervated dogs was associated with greater increases in total peripheral resistance in this group; decreases in cardiac output were similar in the two groups of dogs. Vasopressin decreased heart rate significantly in each group, but the magnitude of the decrease was significantly smaller in cardiac-denervated dogs. In contrast to these results, the intravenous infusion of phenylephrine or angiotensin II in other experiments on the same dogs produced comparable increases in aortic pressure in each group. These results are consistent with earlier evidence indicating that vasopressin elicits more effective reflex mechanisms to attenuate the increases in blood pressure caused by its direct vasoconstrictor action than do other vasoconstrictor agents, such as angiotensin II and phenylephrine. Since the infusion of vasopressin produced a greater increase in arterial blood pressure in cardiac-denervated dogs than it did in sham-operated control dogs, it appears that at least part of the unique action of vasopressin may be mediated by the potentiation of a peripheral vasodepressor reflex arising from cardiac receptors.

Angiotensin II↗
PubMed1989

Effects of norepinephrine and denervation on brown adipose tissue in Syrian hamsters.

Daily injections of either 0.8 or 3.2 mg norepinephrine (NE)/kg for 2 wk failed to stimulate brown adipose tissue (BAT) growth, GDP binding, or cytochrome-c oxidase activity (COA) in Syrian hamsters (Mesocricetus auratus). However, a single injection of 1.6 mg NE/kg produced a small (23%) but significant acute increase in BAT GDP binding without affecting COA. Thus there is some loss of sensitivity to NE with chronic treatment in Syrian hamsters. Unilateral sympathectomy by surgical denervation of the interscapular BAT (IBAT) resulted in decreased GDP binding and COA in the denervated pad. Chronic NE treatment in hamsters with denervated IBAT only partially reversed the denervation-induced decreases in GDP binding and COA. It therefore appears that NE is not solely responsible for the maintenance and stimulation of thermogenic activity and COA in Syrian hamster BAT. Denervation of IBAT also resulted in elevated levels of lipoprotein lipase (LPL) in this tissue, a surprising finding since brown and white adipose tissue LPL activity were both stimulated by chronic NE treatment. Therefore, although NE has a stimulatory effect on LPL activity, the primary influence of the neural input to IBAT on this enzyme is inhibitory. These data exemplify dramatic differences between rats and hamsters in the mechanisms controlling BAT thermogenesis and white and brown adipose tissue LPL activity.

Adipose Tissue, Brown↗
PubMed1991

Effect of acute renal denervation and ANF on renal function in adult spontaneously hypertensive rats.

Experiments were designed to evaluate the influence of the renal efferent nerves on baseline renal function and on the renal response to atrial natriuretic factor (ANF) in euvolemic anesthetized 10- to 12-wk-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) and Munich-Wistar (MW) rats. Acute unilateral renal denervation produced increases in absolute and fractional excretion of sodium and water by the ipsilateral kidney that were similar in SHR and WKY rats; larger responses were observed in MW rats. Excretion by the contralateral innervated kidney was unchanged in each group. Intravenous infusion of ANF (0.25 microgram.kg-1.min-1) caused a diuresis and natriuresis that was similar in the three strains and independent of changes in glomerular filtration rate and renal blood flow. The excretory responses to ANF were larger in denervated than in innervated kidneys. The magnitude of the natriuresis and diuresis produced by ANF was directly related to the pre-ANF rate of urinary excretion, suggesting independent and additive effects of acute renal denervation and ANF on tubular reabsorption. The exaggerated response in the acutely denervated kidney can be explained by removal of a modulatory effect of the renal efferent nerves and associated increases in tubular flow and delivery to more distal ANF-sensitive sites. The denervation responses suggest that the renal efferent nerves have similar effects on sodium and water reabsorption in anesthetized SHR and WKY rats at 10-12 wk of age. The renal nerves and ANF appear to play a larger role in the acute control of sodium and water excretion in MW rats compared to rats of the Okamoto-Aoki strain.

Animals↗
PubMed1994

Effects of sinoaortic baroreceptor denervation on depletion-induced salt appetite.

This study examined the effects of denervation of the carotid sinus and aortic arch baroreceptors on sodium depletion-induced salt appetite in rats. Depletion of extracellular fluid began with two injections of furosemide (10 mg/kg sc), 30 min apart, and removal of all ambient sodium from the cages. Water and sodium-deficient chow were available overnight. The next morning, access to 0.3 M NaCl was provided, and intakes of water and saline were measured every 30 min for 2 h and again at 24 h. Three such tests were administered. Groups of sham and sinoaortic baroreceptor-denervated (SAD) rats had equivalently negative water and sodium balances before access to saline the next morning. Sham-denervated rats drank sufficient saline in 2 h to achieve positive sodium balance and subsequently ingested sodium in excess of need for another 22 h. SAD rats drank half as much saline as sham-denervated rats by 2 and 24 h and remained in negative balance at 2 h. Sham-denervated rats increased their intakes of saline solution with repeated tests, but SAD rats did not. These findings suggest that arterial baroreceptors provide critical neural input for the normal expression of salt appetite.

Animals↗
PubMed2000

Effect of renal denervation on renin gene expression, concentration, and secretion in mature ovine fetus.

To determine the role of the renal nerves on renin secretion and expression in the mature ovine fetus, we performed bilateral renal denervation on eight fetuses of time-dated pregnant ewes (126.8 +/- 0.6 days gestation) and compared renin in them to seven fetuses that underwent sham denervation (126.7 +/- 0.6 days gestation). Fetal arterial and venous catheters were implanted, and after 5-7 days of recovery isoproterenol was infused. Plasma active renin was lower in denervated animals than in intact animals under basal conditions and at each dose of isoproterenol. Plasma prorenin levels were lower in denervated fetuses but unaffected by isoproterenol. Denervation did not change renal renin, prorenin, or renin mRNA, but it did block isoproterenol-induced increases in renin mRNA in renocortical cells in vitro. We conclude that the renal nerves are required for renin secretory mechanisms and responsiveness of renin mRNA to beta-adrenergic stimulation but not for the expression of renin in the fetal kidney. We propose that one or more of the factors that maintain renin expression in the perinatal period may be absent or may be replaced by the renal nerves in the adult.

Animals↗
PubMed1977

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog.

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Animals↗
PubMed1984

Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs.

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

Prostaglandin blockade impairs denervation diuresis and natriuresis in the rat.

Acute unilateral renal denervation of control rats produced an ipsilateral diuresis (5.5 +/- 0.8 to 10.0 +/- 1.0 microliter/min, P less than 0.01) and natriuresis (579 +/- 202 to 2,668 +/- 225 neq/min, P less than 0.01) without a significant change in glomerular filtration rate or effective renal plasma flow. Inhibition of prostaglandin synthesis with indomethacin or meclofenamate (4 mg/kg iv) after acute unilateral denervation eliminated the diuresis (13.3 +/- 1.6 to 5.0 +/- 0.9 microliter/min, P less than 0.01) and attenuated the natriuresis (3,098 +/- 462 to 1,097 +/- 163 neq/min, P less than 0.01). Denervation diuresis and natriuresis were significantly impaired to the same extent when denervation was performed after inhibition of prostaglandin synthesis (3.2 +/- 0.3 to 4.9 +/- 0.4 microliter/min, NS; and 490 +/- 154 to 1,036 +/- 274 neq/min, P less than 0.05 vs. control, respectively). These results indicate that the natriuresis and diuresis seen after acute unilateral denervation in anesthetized rats are highly dependent upon prostaglandins and cannot be initiated or maintained when prostaglandin synthesis is impaired by indomethacin or meclofenamate.

Animals↗
PubMed1992

Denervation inhibits early increase in Na(+)-H+ exchange after uninephrectomy but does not suppress hypertrophy.

Na(+)-H+ exchange in the rat proximal tubule luminal membrane increases approximately 30% within 15 min after the contralateral uninephrectomy. The present study was designed to test whether altered renal sympathetic nerve outflow to the remaining kidney is the underlying mechanism of increased antiport activity and whether suppression of Na(+)-H+ antiport activity by renal denervation inhibits renal hypertrophy in the remaining kidney after uninephrectomy. Sprague-Dawley rats were divided into four groups: 1) sham operated, 2) uninephrectomized, 3) uninephrectomized with prior denervation of the remaining kidney, and 4) contralateral renal denervation. Na(+)-H+ antiport activity (brush-border vesicles), Na(+)-K(+)-ATPase activity (basolateral vesicles), and kidney weight were measured days 1-7. On days 1 and 7, Na(+)-H+ antiport activity and Na(+)-K(+)-ATPase activities were significantly greater in uninephrectomized rats. Denervation of the remaining kidney before contralateral uninephrectomy prevented the stimulation of the antiporter and Na(+)-K(+)-ATPase activity, but failed to inhibit renal hypertrophy by day 7. In separate experiments, contralateral renal denervation alone without removal of the kidney stimulated the Na(+)-H+ antiporter and Na(+)-K(+)-ATPase activity. Kidney weight, however, remained unchanged. The results demonstrate a dissociation between the activation of the Na(+)-H+ antiporter and induction of renal hypertrophy in vivo.

Animals↗
PubMed1975

Glycogen replenishment following exercise: effects of denervation and tenotomy.

To examine the role of the nervous system in the rapid replenishment of muscle glycogen that occurs after exhaustive exercise, glycogen stores and glycogen synthetase activity of normal gastrocnemius muscles of untrained and trained guinea pigs were compared to glycogen and synthetase activity of trained gastrocnemius muscles that were denervated or tenotomized immediately after exhaustive exercise and then allowed to recover for 48 h. The trained tenotomized muscles, but not the denervated muscles, had significantly (P smaller than 0.05) less glycogen than the trained normal muscles. These results suggest that neither nerve impulse conduction nor tropic substances contained in neural tissue proximal to the site of denervation mediate glycogen replenishment after exercise. The active, glucose 6-phosphate independent (I) form of glycogen synthetase activity was reduced by both denervation and tenotomy at 48 h after exercise with no significant (P greater than 0.05) differences detected for the total of I and D (glucose 6-phosphate dependent) synthetase activity. Synthetase I relative to total synthetase activity was similar in trained and untrained normal muscles, both of which had significantly (P smaller than 0.05) greater relative I activities than denervated or tenotomized muscles. These synthetase data show that elevated glycogen stores following recovery from exercise may be observed in the absence of increased levels of glycogen synthetase activity.

Achilles Tendon↗
PubMed1981

Effect of peripheral chemoreceptor denervation on acclimatization of goats during hypoxia.

The purpose of this study was to determine the effect of peripheral chemoreceptor denervation on ventilatory acclimatization of goats during chronic hypoxia. After 1 h of stimulated altitude (PB 450 Torr), arterial O2 tension (PaO2) in seven normal goats averaged 42 Torr, and arterial CO2 tension (PaCO2) was 1.3 Torr below control (P less than 0.001). In these goats nearly 66% of the increase in alveolar ventilation (VA) associated with acclimatization occurred between 1.5 and 4 h of hypoxia. Acclimatization was complete by the 3rd day of hypoxia, and it caused 1) a 23% increase in VA/CO2 output (P less than 0.001); 2) a 5-Torr increase in PaO2 (P less than 0.001); and 3) a 6.5-Torr decrease in PaCO2 (P less than 0.001). Denervation of the carotid chemoreceptors in seven goats caused hypoventilation during eupnea at sea level (PaCO2 change from control +7 Torr, P less than 0.001). Denervation also attenuated but did not eliminate peripheral chemoreceptor responsiveness. No additional changes were observed following attempted denervation of the aortic chemoreceptors. After 1 h of simulated altitude (PB 530 Torr), PaO2 in the denervated goats averaged 46 Torr, and PaCO2 was increased 1.1 Torr above control (P less than 0.001). In these goats VA did not change significantly during the subsequent 3 days of hypoxia. Accordingly, we conclude that the peripheral chemoreceptors are essential for ventilatory acclimatization of goats during chronic hypoxia.

Acclimatization↗
PubMed1981

Denervated and intact kidney responses to exercise in the dog.

In conscious female dogs exercise-induced changes in the function of the innervated and denervated kidney were studied by clearance techniques. The animals were prepared for experiments by chronic unilateral renal denervation and surgical division of the urinary bladder to enable separate urine collection from each kidney. A 20-min run on a treadmill at a speed of 2.6 m/s significantly decreased urine flow, osmolar clearance, sodium excretion, as well as clearances of exogenous creatinine and p-aminohippurate in the denervated kidney only. In dogs running at 3.6 m/s renal hemodynamics decreased significantly and similarly for both kidneys, whereas the fall in renal excretion was virtually limited to the denervated kidney. As glomerular filtration rate (GFR) was falling during exercise, sodium excretion per 100 ml GFR tended to increase in the innervated kidney, in contrast to an expected slight fall on the denervated side. This indicated a defect of tubular sodium reabsorption of the innervated kidney. On the whole, the data do not support an important mediatory role of renal nerves in the mechanism of renal function changes during exercise.

Animals↗