Biomedical subjects

B S Huang

Publications and source records attributed to B S Huang.

At least 37 records · Page 2Linked to original sources

PubMed1998

Brain "ouabain", a neurosteroid, mediates sympathetic hyperactivity in salt-sensitive hypertension.

This review addresses recent developments in the neurobiology of an endogenous inhibitor of brain Na+, K+ - ATPase, "ouabain". "Ouabain" is present in hypothalamic and medullary neurons and mediates sympathoexcitatory and pressor responses to acute and chronic increases in cerebrospinal fluid (CSF) sodium concentration as well as mediates the sympathoexcitatory and pressor responses to high dietary sodium intake in SHR and Dahl-S rats, and sympathetic hyperactivity in the congestive heart failure. Some of these actions of "ouabain" in the CNS take place in the median preoptic nucleus and ventral part of the AV3V region. Despite recent advances in unveiling a biological role for "ouabain" its structure, biosynthetic and metabolic pathways as well as actual control mechanisms remain unresolved.

Animals↗

PubMed1998

Surgery for achalasia: long-term results in operated achalasic patients.

Achalasia is a functional disorder of the alimentary tract due to decreased or absent peristalsis of the esophageal body and obstructive outlet of the esophagus. Surgical treatment, eg. esophagomyotomy of the lower esophageal sphincter (LES), was one choice for resolving the problem and its effect was affirmative from reviews of many internationally authorized articles. However, few reports have ever questioned the long-term effects of it. From January 1968 to May 1996, 159 esophageal achalasic patients, 90 males and 69 females, were admitted due to dysphagia or food regurgitation. One hundred and forty-five patients had received 158 operations related to this benign motor disorder. The majority of patients received either modified Heller esophagomyotomy (M) or M plus modified Belsy Mark IV antireflux procedure (M+W) for primary treatment of their esophageal disorder, while conditional selection with addition of esophageal resection as advanced procedures for failure of primary surgery. We retrospectively studied these patients, collected their preoperative and postoperative clinical results, analyzed the causes of recurrent symptoms, compared the long-term results in different surgical procedures and searched for the pathogenesis of their failure. The results disclosed that the overall success rate for both methods was 73.1% with 85.7% for patients receiving M+W (56) and 64.9% of M (77) only. Through long-term follow-up, we had an improvement rate of 97.4% at an early stage and 53.3% for M at a late stage and 98.4% and 55.6% for M+W, respectively. The postoperative natural course of achalasic patients could be seen and progressive deterioration of the operated patients with time was noted. Several factors might contribute to the causes of unsuccessful surgery. We summarized them as incomplete myotomy, fused or healed myotomy, gastroesophageal reflux (GER), mucosal hernia and co-combined antireflux procedure by hypercalibrated or floppy wrapping. Esophagomyotomy or myotomy plus antireflux procedure for the esophagus could be concluded to rather effective in the long-term but palliative treatments for achalasia chronic deterioration of the results could be found for both of them. Defective myotomy and GER may be the major causes for their failure. The choice of types of surgery between M and M+W was not the cause of the unsuccessful results whereas the operative strategy and procedures would have a certain significance on the long-term effect.

Adolescent↗

PubMed1997

Blockade of brain 'ouabain' prevents the impairment of baroreflexes in rats after myocardial infarction.

BACKGROUND: The purpose of this study was to test whether increased brain "ouabain" contributes to impairment of both arterial and cardiopulmonary baroreceptor reflexes in congestive heart failure (CHF). METHODS AND RESULTS: Two to 5 days after coronary artery ligation (MI) or sham surgery in male Wistar rats, chronic intracerebroventricular (ICV) infusion was started with either antibody Fab fragments, which bind ouabain and related steroids with high affinity, or gamma-globulins as control (200 microg x 12 microL[-1] x d[-1] for both) with osmotic minipumps implanted subcutaneously. After 8 weeks of infusion, in conscious rats, mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), and renal sympathetic nerve activity (RSNA) were recorded at rest and in response to ramp changes in blood pressure (BP) induced by intravenous phenylephrine and nitroprusside and to changes in CVP elicited by acute volume expansion with 5% dextrose. Compared with sham rats, in MI rats with ICV gamma-globulins, resting MAP was significantly lower and CVP increased, and both arterial and cardiopulmonary baroreflex control of RSNA and HR were attenuated. ICV Fab fragments prevented the decrease in resting BP and largely prevented impairment of arterial and cardiopulmonary baroreflex control of both RSNA and HR. CONCLUSIONS: These data indicate that increased brain ouabain plays a major role in the impairment of baroreflexes in rats with CHF after myocardial infarction.

Animals↗

PubMed1997

Sympathoexcitatory effect of hypothalamic/hypophysary inhibitory factor in rats.

We recorded changes in arterial blood pressure, heart rate, and renal sympathetic nerve activity in response to intracerebroventricular injection of bovine hypothalamic/hypophysary inhibitory factor and ouabain in conscious Wistar rats. Ouabain at 0.3 to 0.6 microgram caused dose-related increases in blood pressure, heart rate, and nerve activity (peak increases: 19 +/- 2 mm Hg, 42 +/- 4 beats per minute, and 48 +/- 4%, respectively; P < .05 versus basal). These responses were all blocked by central antibody Fab fragments, which bind ouabain and related steroids with high affinity. The inhibitory factor significantly increased blood pressure but decreased heart rate and nerve activity. Dose-dependent increases in blood pressure as well as heart rate and nerve activity were observed when the inhibitory factor was injected after intravenous injection of the vasopressin antagonist D-(CH2)5Tyr-(Me)AVP. Central Fab fragments, however, did not affect these responses. Both ouabain and the inhibitory factor inhibited Na+,K+-ATPase activity in vitro. Fab fragments blocked this inhibition by ouabain but not by the inhibitory factor. These data indicate that the ouabainlike sympathoexcitatory effect of this factor is masked probably by a potent central effect on vasopressin release. In contrast to rat brain "ouabain," this factor does not exhibit a high affinity for the Fab fragments, supporting the previous finding that this compound is structurally a nonouabain Na+,K+-ATPase inhibitor.

Animals↗

PubMed1997

Surgical treatment of endobronchial tuberculosis.

The incidence of tuberculosis remains fairly high in some developing countries. Endobronchial tuberculosis may cause bronchostenosis, with potentially severe respiratory symptoms, atelectasis and secondary pneumonitis. Thirty-two surgically treated cases of tuberculous bronchostenosis (33 operations) are presented. In 13 cases-segmental resection or lobectomy was performed with bronchoplastic procedures. Anastomotic stenosis necessitated pneumonectomy 5 years later in one of the 13 and one patient had wound infection. Nineteen patients underwent pulmonary resection without bronchoplasty. Apart from the patient with anastomotic stenosis, all 32 were symptom-free in the follow-up period. Forced expiratory volume was significantly improved in the ten tested patients with bronchoplasty. The results suggest that surgical treatment is safe for endobronchial tuberculosis with poor response to specific chemotherapy. In addition to checking progression of the disease, bronchoplasty helps to preserve lung function. Appropriate chemotherapy should be given for 9-12 months perioperatively to prevent recurrence and restenosis.

Adolescent↗

PubMed1997

Leakage of intrathoracic oesophagovisceral anastomoses in adenocarcinoma of the gastric cardia: changes in serial APACHE II scores and their prognostic significance.

OBJECTIVE: To evaluate changes in serial Acute Physiology and Chronic Health Evaluation (APACHE) II scores in patients with intrathoracic oesophageal anastomotic leaks and to assess their prognostic significance. DESIGN: Retrospective study. SETTING: Teaching hospital, Taiwan. SUBJECTS: 18 patients (4%) who developed intrathoracic oesophageal anastomotic leaks in a total of 491 patients who underwent oesophagogastrectomy for adenocarcinoma of the gastric cardia between 1980 and 1994. MAIN OUTCOME MEASURE: APACHE II scores in those that survived (n = 10) compared with those who died (n = 8). RESULTS: Of the 18 patients, 8 (44%) died. The preoperative general condition, biochemical data, and perioperative APACHE II scores were similar in the two groups. Leakage from the oesophageal anastomoses caused similar degrees of sepsis in the two groups in terms of APACHE II scoring, but the APACHE II scores of survivors started to decline within a week of initial management. In contrast, the APACHE II scores of those who died had increased one week after the leak had been diagnosed despite initial management. There were significant differences in the APACHE II scores of survivors and those who died from one week after leakage until discharge or death (p < 0.001). Only one patient (1/9) survived if the APACHE II score one week after diagnosis of the leak was more than 10. None died of the leak if the APACHE II scores were equal to or less than 10 after a week. CONCLUSIONS: Adequate surgical drainage, antibiotic cover according to the microbiological picture, and nutritional support are essential in the management of intrathoracic oesophageal fistulas. Early reoperation to close early leaks by simple suture or secondary wrapping and to improve local drainage is recommended. The APACHE II scoring system is valuable in evaluating the severity of sepsis caused by intrathoracic oesophagovisceral anastomosis leaks and may serve as an indicator of adequate management. Aggressive surgical measures should be considered if APACHE II scores rise during initial management.

APACHE↗

PubMed1996

Sympathoexcitatory and pressor responses to increased brain sodium and ouabain are mediated via brain ANG II.

Intracerebroventricular administration of hypertonic saline, ouabain, brain ouabainlike activity (OLA), or angiotensin II (ANG II) causes sympathoexcitatory and pressor effects in rats. To clarify the possible interaction between increased brain sodium, brain OLA, and the brain renin-angiotensin system (RAS), increases in mean arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA) in response to intracerebroventricular 0.3 M NaCl, ouabain, and ANG II were recorded in conscious Wistar rats before and after intracerebroventricular pretreatment with the angiotensin-receptor (AT1) blocker losartan, antibody Fab fragments (Digibind), or, as control, gamma-globulins. These Fab fragments bind ouabain and brain OLA with high affinity. The arginine vasopressin (AVP) antagonist [d(CH2)5Tyr(Me)]AVP (30 micrograms/ kg) was injected intravenously before each intracerebroventricular injection. Intracerebroventricularly administered 0.3 M NaCl (3.8 mul/min for 10 min), ouabain (0.3 and 0.6 microgram), and ANG II (10 and 30 ng) caused similar pressor responses. However, the extent of HR and RSNA responses to ANG II was smaller than those to 0.3 M NaCl and ouabain. Intracerebroventricular losartan (10 and 20 micrograms) blocked responses to ANG II and 0.3 M NaCl and significantly attenuated the responses to ouabain (pressor response by 50-70%; RSNA and HR by 60-80%). In contrast, intracerebroventricular Fab fragments (66 micrograms) blocked only the responses to 0.3 M NaCl and ouabain and did not affect the responses to ANG II. These results suggest that an acute rise in brain sodium concentration increases brain OLA and the latter exerts its sympathoexcitatory and pressor effects at least partly via activation of the brain RAS.

Angiotensin II↗

PubMed1996

Blockade of brain "ouabain" prevents sympathoexcitatory and pressor responses to high sodium in SHR.

The effects of blockade of brain "ouabain" by central infusion of antibody Fab fragments, which bind ouabain and brain "ouabain" with high affinity, on sodium-sensitive hypertension were studied in spontaneously hypertensive rats (SHR) from 5 to 9 wk of age on high- or regular sodium diet. The Fab fragments or, in controls, gamma-globulins were infused intracerebroventricularly via osmotic minipump. Blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) and their responses to air stress and to the alpha 2-adrenoceptor agonist guanabenz intracerebroventricularly were recorded in conscious rats at 9 wk. In control SHR but not Wistar-Kyoto rats (WKY), high sodium further increased resting mean arterial pressure (171 +/- 3 vs. 141 +/- 4 mmHg in control SHR on regular sodium) and potentiated excitatory and inhibitory responses of BP, HR, and RSNA to air stress and intracerebroventricular guanabenz, respectively. These effects of high sodium were all prevented by intracerebroventricular Fab fragments. In SHR on regular sodium or WKY on either diet, the Fab fragments had no effects on resting BP or responses to air stress and guanabenz. We conclude that similar to Dahl salt-sensitive rats, in SHR, a sodium-induced increase in brain "ouabain" is responsible for the decreased sympathoinhibition and increased sympathoexcitation and thus the exacerbation of hypertension. Brain "ouabain" appears not to be involved in the development of hypertension in SHR on regular sodium intake.

Air↗

PubMed1996

Brain "ouabain" and angiotensin II in salt-sensitive hypertension in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) received from 5 to 9 weeks of age a high or regular sodium diet and concomitant intracerebroventricular infusions via minipumps of the following compounds: antibody Fab fragments (200 micrograms/d), which bind ouabain and related steroids with high affinity; the angiotensin II (Ang II) type 1 receptor blocker losartan (1 mg/kg per day); a combination of Fab fragments and losartan; and as control, gamma-globulins (200 micrograms/d). The same doses of Fab fragments and losartan were also given intravenously. At 9 weeks of age, compared with SHR on regular sodium, SHR on high sodium that were treated with gamma-globulins had higher resting blood pressure and showed significantly enhanced excitatory responses of blood pressure, renal sympathetic nerve activity, and heart rate to air stress and inhibitory responses to the central alpha 2-agonist guanabenz. Central Fab fragments and losartan alone or combined prevented all these effects of high sodium. Intravenous Fab fragments or losartan was ineffective. Compared with control SHR on high sodium, SHR on high sodium that were treated with Fab fragments had significantly increased sympathoexcitatory and pressor responses to central Ang II injection, consistent with a decrease in brain Ang II receptor occupancy. These data indicate that both increased brain "ouabain" and Ang II contribute to salt-sensitive hypertension in SHR. Brain Ang II receptor stimulation appears to be downstream of "ouabain" in the pathways mediating sympathoexcitatory and pressor effects of high sodium.

Angiotensin II↗

PubMed1995

Dietary Na+ and cardiopulmonary baroreflex control of renal sympathetic nerve activity in SHR.

In young Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with or without chronic sinoaortic denervation (SAD), we evaluated the effects of low, regular, and high dietary sodium intake (L-Na, R-Na, and H-Na, respectively) from 4 to 8 wk of age on cardiopulmonary baroreflex function, which was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) in response to acute volume expansion. In intact SHR H-Na increased blood pressure (BP), whereas L-Na decreased BP. No changes were observed in intact WKY. The gain of the cardiopulmonary baroreflex control of both HR and RSNA was significantly attenuated in SHR vs. WKY on R-Na. In both SHR and WKY, L-Na had no effects on the gain of RSNA and HR responses. In both strains, H-Na did not affect the gain of HR but attenuated the gain of the RSNA response. H-Na attenuated the gain of RSNA response more in SHR with SAD vs. intact SHR (52 vs. 69% of corresponding R-Na control) but less in WKY with SAD vs. intact WKY (80 vs. 71% of corresponding R-Na control). These data indicate that in SHR, H-Na further desensitizes the already impaired cardiopulmonary baroreflex control of RSNA. After SAD, this attenuation is more prominent in SHR but becomes less prominent in WKY. High sodium intake, therefore, modulates the interaction between the arterial and cardiopulmonary baroreflexes in the control of RSNA oppositely in WKY vs. SHR.

Animals↗

PubMed1995

Brain 'ouabain' and desensitization of arterial baroreflex by high sodium in Dahl salt-sensitive rats.

In Dahl salt-sensitive (S) rats, high sodium intake further desensitizes arterial baroreflex function. To assess the possible involvement of brain "oubain," we gave Dahl S rats a regular or high sodium diet from 4 to 7 weeks of age and administered intracerebroventricular antibody Fab fragments, which bind ouabain with high affinity, or gamma-globulins as control (200 micrograms/12 microL per day for both) using osmotic minipumps. We assessed arterial baroreflex function by plotting changes in renal sympathetic nerve activity or heart rate against changes in mean arterial pressure of conscious rats elicited by intravenous phenylephrine and nitroprusside. Dahl S rats on high sodium treated with gamma-globulins showed a significantly higher resting mean arterial pressure versus other rats (130 to 140 versus 95 to 105 mm Hg). In rats treated with gamma-globulins, high sodium desensitized baroreflex control of renal sympathetic nerve activity compared with rats on regular sodium (average gain: -1.88 +/- 0.12 versus -2.73 +/- 0.13, P < .05). In contrast, in rats treated with Fab fragments, high sodium did not increase blood pressure and did not desensitize but slightly sensitized reflex control of renal sympathetic nerve activity. Changes in reflex control of heart rate were similar to those of renal sympathetic nerve activity. These data indicate that blockade of brain "oubain" prevents sodium-induced hypertension as well as the desensitization of the arterial baroreflex in Dahl S rats. Increased brain "oubain" may desensitize the arterial baroreflex and thereby facilitate the hypertension in Dahl S rats on high sodium.

Animals↗

PubMed1995

Brain 'ouabain,' sodium, and arterial baroreflex in spontaneously hypertensive rats.

To assess the possible role of brain "ouabain" in modulating arterial baroreflex function in salt-sensitive hypertension, arterial baroreflex control of renal sympathetic nerve activity and heart rate was evaluated in conscious spontaneously hypertensive rats and compared with that in Wistar-Kyoto rats. A regular sodium or high sodium diet was provided from 5 to 9 weeks of age, with intracerebroventricular infusion of antibody Fab fragments, which bind ouabainlike substances with high affinity, or, as control, nonspecific gamma-globulins (200 micrograms.12 microL-1.d-1 for both). Baroreflex function was assessed by plotting changes in renal sympathetic nerve activity or heart rate against changes in mean arterial pressure by phenylephrine and nitroprusside. In control Wistar-Kyoto rats, high sodium intake did not increase resting blood pressure but sensitized baroreflex control of renal sympathetic nerve activity. In control spontaneously hypertensive rats, high sodium intake significantly increased blood pressure but did not enhance renal sympathetic nerve activity responses. However, in spontaneously hypertensive rats given high sodium diets and treated with Fab fragments, blood pressure did not increase and the baroreflex control of renal sympathetic nerve activity was sensitized significantly. We conclude that in spontaneously hypertensive rats, increase of central "ouabain" by high sodium intake prevents an increase in the sensitivity of arterial baroreflex control of renal sympathetic nerve activity, as observed in Wistar-Kyoto rats on high sodium diets.

Animals↗

PubMed1995

Brain 'ouabain' mediates sympathetic hyperactivity in congestive heart failure.

In congestive heart failure (CHF), endogenous compounds with ouabainlike activity (OLA) may contribute to the maintenance of the circulatory homeostasis by peripheral as well as central effects. In the present study, we assessed changes in peripheral (plasma and left ventricle) and central (pituitary, hypothalamus, pons, and cortex) OLA in two animal models of CHF and determined whether brain OLA mediates sympathetic hyperactivity in CHF. Cardiomyopathic hamsters with their controls were studied at 9 months of age for tissue OLA. Rats were studied 4 weeks after acute coronary artery ligation for tissue OLA and sympathetic activity. In both models, left ventricular end-diastolic pressure was markedly increased. CHF was associated with significant increases in both plasma and tissue OLA in both models. In the brain, the most marked (twofold to threefold) increases occurred in the hypothalamus. In vitro, all OLA measured could be blocked by antibody Fab fragments (Digibind). Conscious rats with CHF showed elevated plasma catecholamines and enhanced responses of mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) to air stress and to intracerebroventricular (ICV) injection of the alpha 2-adrenergic receptor agonist guanabenz compared with sham-operated rats. ICV administration of the Fab fragments did not change resting RSNA or responses to air stress at 1 hour. However, 18 hours after injection of the Fab fragments, resting RSNA levels had significantly decreased compared with the control values, and plasma catecholamine levels had decreased to control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Emergency surgical intervention for severe corrosive injuries of the upper digestive tract.

BACKGROUND: In treating severe corrosive injury of the esophagus and stomach, prompt diagnosis, adequate fluid resuscitation and warranted surgical intervention are the most important factors in rescue of critically ill patients. The purpose of this study was to evaluate the need for, and the advantages of, a surgical approach to treatment of such corrosive injuries to the upper gastrointestinal (UGI) tract, as well as to select the most suitable technique to achieve a good survival rate. METHODS: From January 1983 to December 1991, 220 patients were treated for caustic ingestion injury to the UGI tract. A retrospective review of their records allowed targeting of 27 patients with severe corrosive injury that surgical intervention was required. In this study, peritoneal sign was taken as the key indicator for early emergency operation. The age, sex, elapsed time from injury to operation, the sort and quantity of caustic agent used, injury mechanism, clinical manifestations, alternative surgical treatment methods and causes of death were also reviewed and analyzed in this study. RESULTS: The patients included 13 men and 14 women, of whom the majority were adults (96.3%) who had attempted suicide (85.2%). All of them had taken liquid corrosive agents, usually hydrochloric acid (63%). Eighteen underwent emergency operations; the other nine received only supportive treatment, given their terminal status. The mortality rates for patients with surgery and supportive treatment were 66.7% and 100%, respectively. Four patients died after undergoing esophagectomy with resection of the stomach using the thoracoabdominal method. Only three of the eight patients who received esophageal stripping combined with resection of the stomach through the abdomen died (37.5%). CONCLUSIONS: The time elapsed between injury and development of peritoneal sign is a good indicator of the severity and extent of the injury. When peritoneal sign manifests at a very early stage, it is an indicator that the corrosive injury is very advanced in its progress and that, no matter what procedures were performed, the outcome would be the same. Yet if there were a six-hour gap then aggressive surgical management can rescue some patients. It is recommended based on experience here, that when using the surgical approach, resection of the stomach with stripping of the esophagus is superior to the thoracoabdominal method.

Adolescent↗

PubMed1994

Tumor recurrence in long-term survivors after treatment of carcinoma of the esophagus.

To evaluate the status of tumor recurrence and the possible factors relevant to tumor recurrence among patients who survived more than 5 years after subtotal esophagectomy for the treatment of squamous cell carcinoma of the esophagus, a total of 104 patients who received treatment between 1959 and 1986 were reviewed. In 18 of these 104 patients, local or distant tumor recurrence developed, for a tumor recurrence rate of 17.3%. Eleven (61.1%) of these 18 patients eventually died of carcinomatosis despite further radiotherapy or chemotherapy, or both, and 4 patients with the disease are still alive. Three patients continue to survive after aggressive therapy was instituted for control of the locally recurrent tumor. Sixty-nine of the 104 patients are alive without tumor recurrence after the initial esophagectomy, and the remaining 17 patients died of miscellaneous causes. Tumor recurrence appears to be the most important factor affecting the prognosis in long-term survivors with resectable esophageal carcinoma. Among the 11 patients who died of tumor recurrence, 10 died within 5 to 9 years of their esophagectomy. The incidence of various modes of tumor recurrence among these 18 patients was as follows: blood-borne metastasis, 61%; lymph node recurrence, 33%; and locoregional organ recurrence, 33%. Factors that may be pertinent to a higher tumor recurrence rate include male sex, moderate to poor tumor differentiation, the presence of lymph node metastasis, and late stage of disease (stage IIb or worse). However, we could not find any statistical significance among these possible factors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1994

Dietary Na and baroreflex modulation of blood pressure and RSNA in normotensive vs. spontaneously hypertensive rats.

Different changes in baroreflex control of the circulation have been postulated to play a role in the different blood pressure (BP) effects of dietary sodium in normotensive vs. genetically hypertensive rats. We therefore evaluated in young Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with or without chronic sinoaortic denervation (SAD), the effects of low, regular, and high dietary sodium intake from 4 to 8 wk of age on BP and baroreflex function. The latter was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate in response to (de)pressor agents. In SHR, the above range of sodium caused a marked change in resting BP, somewhat more in intact (48 mmHg) vs. SAD (36 mmHg) rats. In contrast, in WKY this range of sodium intake caused only a minor (7 mmHg) change in resting BP of intact WKY but a significant (16 mmHg) change in WKY with SAD, mainly due to an increase in BP on high sodium. In intact WKY increasing dietary sodium from low to regular to high caused stepwise increases in the gain of the RSNA-BP reflex, whereas in intact SHR only an increase from low to regular sodium intake increased the gain. After SAD, the gain of the RSNA-BP reflex was very low, and no longer affected by dietary sodium in either strain. These data suggest that in WKY a sensitization in arterial baroreflex control of RSNA prevents a sodium-induced increase in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1994

Chronic central versus peripheral ouabain, blood pressure, and sympathetic activity in rats.

To assess whether chronic ouabain administration causes hypertension by increasing sympathetic activity, we recorded arterial blood pressure and heart rate at rest and after ganglionic blockade in conscious Wistar rats following 10 to 14 days of central or peripheral administration of ouabain. Intracerebroventricular or intravenous infusion of ouabain (10 micrograms/d for both) as well as subcutaneous ouabain pellets (releasing 25 micrograms ouabain/d per pellet) increased mean arterial pressure by 20 to 30 mm Hg and heart rate by 40 to 60 beats per minute. Ouabain pellets increased blood pressure and heart rate in a dose-related manner. After 2 weeks of all ouabain treatments, ouabainlike activity in plasma was not changed but increased significantly in hypothalamus and adrenals. Ouabainlike activity in the adrenals was increased more by intravenous than subcutaneous or intracerebroventricular ouabain treatment, but the different treatment modes caused similar increases in the hypothalamus. Concomitant central infusion of antibody Fab fragments against ouabain prevented the ouabain pellet-induced increases in blood pressure and heart rate. Ganglionic blockade by intravenous hexamethonium normalized blood pressure and heart rate in ouabain-treated rats. These data suggest that in normotensive rats exogenous ouabain, regardless of the mode of administration, may act centrally to cause sympathoexcitation and thus hypertension.

Animals↗

PubMed1994

Brain "ouabain" mediates the sympathoexcitatory and hypertensive effects of high sodium intake in Dahl salt-sensitive rats.

To assess whether brain ouabain-like activity (OLA) mediates the hypertensive effects of high sodium intake in Dahl salt-sensitive (Dahl S) rats, the effects of blockade of brain OLA on mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were evaluated in conscious Dahl salt-resistant (Dahl R) and Dahl S rats on a regular (120 mumol/g) or high sodium (1370 mumol/g) diet from 4 to 7 weeks of age. Dahl S rats given high sodium showed higher basal MAP and augmented responses of MAP and RSNA to air stress and to intracerebroventricular injection of the alpha 2-adrenergic receptor agonist guanabenz as compared with Dahl R rats or Dahl S rats given regular sodium. In contrast, the sympathoexcitatory and pressor responses to intracerebroventricular injection of ouabain (0.3 and 1.0 microgram) were markedly attenuated in Dahl S rats given high sodium. Intracerebroventricular preinjection of 0.3 microgram ouabain significantly enhanced blood pressure and RSNA responses to air stress and intracerebroventricular guanabenz in Dahl S rats given regular sodium to the levels observed in Dahl S rats given high sodium. Intracerebroventricular digoxin-specific antibody Fab (DAF) fragments (132 micrograms/8 microL for 5 minutes) did not change basal MAP and RSNA during the first 4 hours after administration in Dahl S rats on a high sodium diet for 3 weeks. However, 18 hours after the injection of DAF fragments, basal MAP and RSNA were significantly decreased, reaching values for Dahl S rats on a regular sodium diet. The magnitude of increases or decreases in MAP and RSNA to air stress or intracerebroventricular guanabenz were significantly attenuated by the DAF fragments in Dahl S rats on a high sodium but not regular sodium diet. Concomitant intracerebroventricular infusion of DAF fragments (200 micrograms per day) prevented the development of hypertension after a high sodium diet in Dahl S rats and prevented an augmentation in pressor and sympathoexcitatory responses to air stress. After discontinuing the infusion of DAF fragments, resting MAP gradually increased to the high levels found in Dahl S rats given high sodium treated with gamma-globulins. These results support the concept that high sodium intake may cause hypertension in Dahl S rats by increasing endogenous brain OLA, thereby enhancing sympathetic outflow and basal blood pressure as well as sympathoexcitatory and pressor responses to stress.

Animals↗